Intraocular pressure (IOP) is the fluid pressure of the eye. As pressure is a measure of force per area, IOP is a measurement involving the magnitude of the force exerted by the aqueous humor on the internal surface area of the anterior eye. The IOP can be theoretically determined by the Goldmann equation, which is IOP = (F/C) + P, where F represents aqueous flow rate, C represents aqueous outflow, and P is the episcleral venous pressure. A change or fluctuation in any of these variables will inevitably alter the IOP.
Intraocular pressure is carefully regulated, and disturbances are often implicated in the development of pathologies such as glaucoma, uveitis, and retinal detachment. IOP exists as a fine-tuned equilibrium between the production and drainage of aqueous humor. The balance between IOP increases with increased systemic blood pressure. Sudden increases in IOP can cause mechanical stress and ischemic effects on the retinal nerve fiber layer, while sudden decreases in IOP can cause micro-bubbles to form from dissolved gases in microvasculature with resultant gas emboli and ischemic tissue damage. Chronic elevation of IOP has been infamously implicated in the pathogenesis of primary open-angle glaucoma (POAG) and other vision-damaging problems.
In approaching intraocular pressure, a basic understanding of the production and outflow of the aqueous humor is helpful. Aqueous humor is produced by the ciliary epithelium of the iris ciliary body pars within the posterior chamber of the anterior eye. Aqueous humor accumulates in the posterior chamber and flows through the pupil into the anterior chamber. Aqueous humor then exits the anterior chamber via one of three routes:
- The vast majority of aqueous humor drains through the trabecular meshwork at the angle of the anterior chamber and into the Schlemm canal where it enters episcleral veins.
- A small amount of the aqueous humor passes into the suprachoroidal space and enters venous circulation in the ciliary body, choroid, and sclera.
- A still smaller amount of aqueous humor transits through the iris and back into the posterior chamber.
An intricate and elegant homeostatic mechanism maintains intraocular pressure. Acutely, the sympathetic nervous system directly influences the secretion of aqueous, with beta-2 receptors causing increased secretion and alpha-2 receptors causing decreased secretion. Homeostatic regulation of IOP, however, relies primarily on the regulation of aqueous outflow through the trabecular meshwork. This regulation occurs through modulation of the resistance of the TM outflow tract in the juxtacanalicular region (region bordering SC), likely at the level of the inner wall basement membrane. IOP forces produce mechanical stress of the cells of this layer, which initiates a signal cascade leading to increased activity of matrix metalloproteinases (specifically MMP14 and MMP2) with a resultant increase in cell turnover at the level of the TM, allowing increased aqueous humor outflow.
Intraocular pressure is traditionally measured by applanation tonometry, which gives an estimate of the pressure inside the anterior eye based on the resistance to flattening of a small area of the cornea. Pressures of between 11 and 21 mmHg are considered normal, and diurnal variance of IOP is expected, with higher pressures typically found in the morning. While the mainline modality for measurement of IOP remains Goldmann applanation tonometry (GAT), rebound tonometry using portable tonometers has emerged as a practical measurement of IOP in the acute setting. These two modalities, however, are not exchangeable according to current research. More recently has seen the development of microelectromechanical and nanoelectromechanical systems for 24-hour monitoring of intraocular pressure. While larger studies are required to validate their safety and efficacy, these newer systems will play a large role in the management and monitoring of patients with pressure-related pathology.
Limitations exist in applanation technology due to reliance on the Imbert-Fick principle, which presumes that pressure within a sphere is equal to the force necessary to flatten its surface divided by the area flattened. This principle does not take into account the inherent rigidity or biomechanical properties of the corneal wall. Indeed, it only works in this context because the force of capillary attraction of the tear meniscus opposes corneal rigidity when the flattened area is 3.06 mm in diameter. If, for example, the corneal wall is exceptionally thick, a large force will be required to flatten it; but this force may not correspond to an elevated IOP, resulting in an overestimation of IOP. For this reason, the measurement of central corneal thickness is critical for accurate measurement of IOP.