Intraocular pressure (IOP) is determined by the balance between the amount of aqueous humor produced in the eye and the resistance to its outflow. It is expressed by the Goldmann equation Po = (F/C) + Pv (Po: IOP [mmHg], F: aqueous humor production rate, C: outflow facility, Pv: episcleral venous pressure).
The association between elevated IOP and vision loss from glaucoma has been noted since the 17th century. In the 19th century, William Bowman developed a method to estimate ocular hardness by palpation through closed eyelids. Subsequently, objective tonometry devices were developed, and it was found that only about 2% of the population had IOP exceeding 21 mmHg. This led to the concept that “>21 mmHg is abnormal,” but later studies revised this notion.
The Ocular Hypertension Treatment Study (OHTS) examined the effect of IOP-lowering treatment in 1,636 patients with ocular hypertension5). The treatment group achieved an average IOP reduction of 22.5%5). Over 5 years of follow-up, 9.5% of the untreated group developed glaucoma compared to 4.4% in the treated group. Although IOP reduction decreased the risk of progression to glaucoma, the majority of ocular hypertension patients did not develop damage within 5 years.
Multiple population-based studies have shown that the prevalence of primary open-angle glaucoma (POAG) increases with higher IOP levels3). In the Baltimore Eye Survey, at an IOP of 30 mmHg, approximately 7% of whites and 25% of African Americans had POAG3). Elevated IOP is the only proven modifiable risk factor for glaucoma, with myopia and corneal hysteresis also identified as high-evidence risk factors2).
QCan glaucoma occur even if intraocular pressure is normal?
A
Population-based studies have shown that glaucomatous optic neuropathy can occur even when intraocular pressure is within the statistically normal range (≤21 mmHg). This is called normal-tension glaucoma (NTG). There is considerable individual variation in the susceptibility of the optic nerve to pressure; in some patients, the optic nerve is damaged even at low pressure levels. Randomized controlled trials have shown that lowering intraocular pressure slows the progression of glaucoma even when baseline pressure is in the normal range, and pressure reduction is an effective treatment strategy for all types of glaucoma.
Applanation tonometry is based on the Imbert-Fick law, which states that the internal pressure of an ideal thin-walled sphere is equal to the force required to flatten its surface divided by the area flattened (P = F/A).
GAT is the most frequently used tonometer and is the current reference standard 1)5). It measures the force required to flatten a corneal area of 3.06 mm in diameter. At this diameter, corneal rigidity (resistance) and the surface tension of the tear film (capillary attraction) cancel each other out. In Goldmann’s design, an average corneal thickness of 520 μm was assumed as the condition for offsetting surface tension and corneal rigidity.
With an applanated area of 15.09 mm² (diameter 3.06 mm), the change in intraocular volume during applanation is very small, minimizing the influence of ocular rigidity. Since the surface tension of tears and ocular rigidity are nearly balanced, the Imbert-Fick law can be applied.
Measurement procedure: Instill a topical anesthetic (0.4% oxybuprocaine) and stain the ocular surface with fluorescein. Insert a blue filter into the slit lamp microscope, open the slit width fully, and illuminate from a 60° angle. Read the intraocular pressure when the inner edges of the two semicircles of the applanating prism split image just touch. Intraocular pressure (mmHg) is calculated as applanation force (g) × 10.
Factors affecting the accuracy of GAT include excessive or insufficient fluorescein in the tear film, high astigmatism, corneal irregularity or scarring, eyelid pressure during measurement, and Valsalva maneuver 1). To prevent infection, chemical disinfection or use of disposable prism heads is recommended 1). Accuracy should be checked monthly using a calibration verifier.
This is a portable version of the GAT, with a built-in counterbalance that allows intraocular pressure measurement regardless of body position 1). The measurement principle is the same as GAT, but the tonometer is prone to insufficient fixation, requiring skill to measure. It is useful for supine patients and in the operating room.
It uses an air column of gradually increasing intensity as the applanation force. The force at the moment the cornea is flattened is recorded and converted to mmHg. No topical anesthesia is required, and paramedical staff can perform the measurement.
The accuracy of non-contact tonometers is inferior to GAT. Accurate measurement is not possible in cases of corneal epithelial damage or corneal edema. The measurement time is as short as 1–3 milliseconds, making it susceptible to pulse wave effects from the heartbeat; therefore, at least three measurements should be taken and the average used as the intraocular pressure value. It is reasonably accurate in the normal pressure range, but tends to read lower in high pressure ranges and higher in low pressure ranges. If abnormal values are found, re-examination with GAT is necessary.
This is a new type of non-contact tonometer. After recording the applanation point, the air column continues to be emitted, and the pressure difference between two applanation points when the cornea returns to the applanation point after indentation is measured. This difference reflects corneal hysteresis (an indicator of viscoelasticity). The intraocular pressure “corrected” for high or low corneal elasticity is said to be less dependent on central corneal thickness than other applanation tonometers.
QWhy is the amount of fluorescein important when measuring with the Goldmann applanation tonometer?
A
The amount of fluorescein directly affects the thickness of the tear meniscus and changes the reading of intraocular pressure. Excessive fluorescein thickens the fluorescent ring, altering the position where the inner edges of the two semicircles meet, leading to overestimation of intraocular pressure. Conversely, insufficient fluorescein makes the ring thinner, leading to underestimation. The appropriate staining width is approximately one-tenth of the semicircle diameter.
3. Other methods of intraocular pressure measurement
Schiotz tonometer: A curved footplate is placed on the cornea of a supine patient, and intraocular pressure is calculated from the indentation depth of a weighted plunger. The indentation depth is inversely proportional to intraocular pressure.
Pneumotonometer: A convex silicone tip at the end of a piston riding on an air stream indents the cornea. The pressure when the cornea and tip become flat equals intraocular pressure. In the normal pressure range, it shows good correlation with GAT.
Tono-Pen: A portable device that uses both applanation and indentation principles. Based on the MacKay-Marg theory, it calculates intraocular pressure from the change in strain gauge voltage upon corneal contact. Useful for measuring IOP in patients who cannot sit upright and in children.
Rebound and Dynamic Contour Tonometers
iCare rebound tonometer: A plastic ball 1.8 mm in diameter is fired at the cornea using an electromagnetic field, and IOP is calculated from the deceleration after impact. No anesthesia is required, and it shows good agreement with GAT and Tono-Pen. It is affected by central corneal thickness, and effects of corneal hysteresis and corneal resistance factor have also been reported.
Pascal dynamic contour tonometer (DCT): Uses a piezoelectric sensor to measure dynamic pulsatile fluctuations in IOP. Unlike GAT, it is said to be less affected by central corneal thickness, corneal curvature, and rigidity. It can also measure ocular pulse amplitude. A disposable cover is used, and a Q value indicating measurement quality is displayed digitally.
Central corneal thickness is a parameter that affects the accuracy of many tonometers1). In thin corneas, IOP is underestimated, and in thick corneas, it is overestimated1)3). The change in IOP per 10 μm of central corneal thickness is approximately 0.2 mmHg. However, note that increased thickness due to corneal edema is an exception and leads to underestimation.
Thin central corneal thickness is associated with an increased risk of progression from ocular hypertension to glaucoma and an increased risk of glaucoma progression1)4). However, no generally accepted correction formula exists, and the World Glaucoma Association IOP consensus states that correction factors should not be applied to individual patient measurements3)4). Corneal hysteresis provides additional independent information related to the risk of primary open-angle glaucoma3)4).
All tonometers that applanate the cornea are affected by corneal biomechanical properties1)5). In addition to geometric factors such as thickness and curvature, material properties such as stiffness and viscoelasticity are involved1). This effect is greater in tonometers that applanate the cornea quickly, such as air-puff tonometers and rebound tonometers1).
The physical properties (deformability) of the cornea have a greater impact on IOP measurement accuracy than differences in central corneal thickness or corneal curvature radius. ORA and Corvis ST are tonometers developed to account for these corneal physical properties.
After RK, PRK, and LASIK, intraocular pressure is measured lower than actual. The main causes are flattening of corneal curvature in RK and thinning of the central cornea in PRK and LASIK. In LASIK, IOP is measured 0.3–0.4 mmHg lower per 10 μm of corneal ablation. In patients who have undergone corneal laser surgery for myopia correction, IOP measurements may significantly underestimate true IOP, requiring careful visual field and OCT monitoring 1).
In the supine position, IOP is 3–5 mmHg higher than in the sitting position, and this difference is particularly large in glaucoma patients. Postural changes are attributed to changes in episcleral venous pressure. Measurement of diurnal variation including body position during nighttime sleep is increasingly emphasized.
All tonometers have inter- and intra-observer variability in measurements 1)5). For follow-up of the same patient, the same tonometer should be used 1)5).
5. Setting and Management of Target Intraocular Pressure
Target intraocular pressure is set as the upper limit of IOP that sufficiently delays the progression of visual field deterioration to maintain the patient’s quality of life (QoL) 1)5). There is no single target IOP level appropriate for all patients; it must be individually set for each eye of each patient 1)5).
Criteria for Setting Target Intraocular Pressure
Early glaucoma: 18–20 mmHg, with a reduction of 20% or more from baseline as a guideline 5).
Moderate glaucoma: 15–17 mmHg, with a reduction of 30% or more from baseline required 5).
Advanced glaucoma: A lower target intraocular pressure is necessary.
Reassessment: Target intraocular pressure should be reviewed at each follow-up, and further adjustments should be made if progression is confirmed or if other ocular or systemic diseases develop 1)5).
Factors Influencing Target Intraocular Pressure
Age: Younger patients require a lower target due to longer life expectancy, while older age is a risk factor for faster progression 1).
Untreated intraocular pressure: The lower the untreated IOP, the lower the target IOP may need to be 1).
Rate of progression: The faster the progression, the lower the target IOP should be set 1).
Others: Pseudoexfoliation, central corneal thickness, status of the fellow eye, family history, adverse events of treatment interventions, and patient preferences should be comprehensively considered 1).
Greater initial visual field damage is the most important predictor of glaucoma-related blindness 1). Since the rate of progression is unknown at the time of initial diagnosis, target IOP is set based on risk factors, and after sufficient follow-up of usually 2–3 years, the target IOP is readjusted using the rate of progression 1).
QWhat should be done if the target intraocular pressure is achieved but glaucoma is progressing?
A
If glaucoma progresses despite reaching the target intraocular pressure, the target pressure should be reset lower and treatment changed. Discuss with the patient the risks and benefits of additional interventions. Conversely, if the target pressure has not been reached but glaucoma is stable, the target may be revised upward. Target intraocular pressure is not fixed; it is a concept dynamically reassessed over time.
Intraocular pressure is a dynamic parameter, fluctuating 4–5 mmHg even in healthy individuals, and more so in glaucoma patients. Development of monitoring technologies beyond in-office measurements is progressing.
Early animal studies investigated surgical implantation of pressure transducers or intraocular sensors in the lens capsule, but surgical risks were a major drawback. For temporary monitoring, a soft contact lens sensor (CLS) that measures changes in ocular dimensions over 24 hours has been developed. In vitro studies show good correlation with true intraocular pressure, and it is approved for clinical use in Europe. However, difficulty interpreting large amounts of data and inability to directly convert output signals to mmHg are major limitations.
European Glaucoma Society. European Glaucoma Society Terminology and Guidelines for Glaucoma, 6th Edition. Br J Ophthalmol. 2025.
Foo B, Aung T, et al. Risk factors and biomarkers associated with glaucoma: an umbrella review of meta-analyses. Invest Ophthalmol Vis Sci. 2025;66(12):35.
American Academy of Ophthalmology. Primary Open-Angle Glaucoma Preferred Practice Pattern. 2024.
American Academy of Ophthalmology. Primary Open-Angle Glaucoma Suspect Preferred Practice Pattern. 2024.
European Glaucoma Society. European Glaucoma Society Terminology and Guidelines for Glaucoma, 5th Edition. Br J Ophthalmol. 2020.
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