It is well-known that IOP is a single, modifiable factor in determining the risk and further progression of glaucoma. As IOP is a measurement we use consistently in practice, it is worth learning about the roles the other pressures, namely, ocular perfusion pressure (OPP), cerebrospinal fluid pressure (CSFP) and blood pressure (BP), play in measuring IOP. (See “IOP: A Review,” p.20.)

Here’s a look at these pressures and the current action step associated with all of them.

OPP

In simple terms, OPP refers to the amount of blood flow delivered to ocular tissues. It is calculated as the difference between arterial BP and venous BP. Thus, OPP also can be thought of as the difference between arterial BP and IOP because IOP is similar to the value of venous BP. The exact formula to calculate OPP is: Mean OPP=2/3(diastolic BP+1/3(systolic BP/diastolic BP)-IOP.

A specific balance between arterial BP and venous BP is required to have adequate perfusion for any tissue. Ischemia results when tissues fed by blood vessels have poor perfusion. Therefore, an imbalance between arterial BP and venous BP can have devastating consequences on the optic nerve and, thus, has been linked to glaucomatous damage.¹

The significance of OPP is that it has been linked with open-angle glaucoma in many population-based epidemiologic studies in the United States, Europe and Caribbean.

Specifically, a low diastolic perfusion pressure below 55 mmHg, was associated with open-angle glaucoma.^2-5 The severity of normotensive, more recently called low-tension open-angle glaucoma, was strongly correlated with the circadian fluctuation of OPP.⁶ Also, the Early Manifest Glaucoma Trial indicates that a low systolic perfusion pressure at baseline reveals faster progression of glaucoma.^7,8

CSFP

CSFP is the true counter-pressure to IOP across the lamina cribrosa. Both the IOP and CSFP are important factors in determining the pliability of the optic nerve.¹ Meaning, the IOP is the force pushing against the lamina cribrosa, and the CSFP pushes back. With a low CSFP or a high IOP, there is an imbalance in forces, which can result in deformation of the optic nerve head, known as cupping.

Imagine, for a moment, diving deep into the ocean. You can feel the atmospheric pressure increasing around you, as you go deeper. Your IOP is extremely high at significant depths, but because of your body’s autoregulation, your CSFP increases as well, maintaining the equilibrium and, therefore, this action does not cause an acute onset of glaucoma or permanent damage to the optic nerve. Thus, this balance always must be working to allow for proper nourishment of the optic nerve in a healthy, stress-free environment.²

BP

BP is the pressure of the blood running through the circulatory system. It is affiliated with the heartbeat’s force and rate, as well as the arterial walls’ diameter and elasticity. Although the possible interactions of BP with IOP and glaucoma have been studied, the results are somewhat contradictory:

On the one hand, hypertension has been linked to a high IOP. Specifically, cross-sectional studies have suggested that each 10 mmHg higher systolic BP is related to 0.23 mmHg to 0.32 mmHg increase in IOP.^2,4,11 These are similar to the values found in longitudinal studies, including the Beaver Dam and Barbados Eye Studies.^12,13 That said, there has been no direct correlation to the onset of glaucomatous damage or progression.

On the other hand, low BP results in low OPP, which has been linked to inciting glaucomatous damage in addition to hastening progression rates of glaucoma. OPP is dependent on a complex process involving both IOP and BP, as explained above. Vascular dysregulation disrupts the equilibrium of arterial and venous pressures, which leads to ischemia. This has been proposed as a “vascular theory” for the underlying cause of glaucoma.^14-16 As is the case with other diseases, such as diabetes, in which fluctuation in blood sugar is often more damaging than stable blood sugar, wide fluctuations in OPP also occur in situations of vascular dysregulation and seem to occur mostly at night when OPP is the lowest.

This is particularly relevant in normotensive glaucoma (NTG). In a study looking at nocturnal systemic hypotension and the risk of glaucoma progression, it was revealed that both the magnitude and duration of nocturnal hypotension is related to VF progression in patients who have NTG.¹⁷

The take home: Patients who show glaucoma progression, despite adequate and stable IOP decreases with reported compliance of their medications, specifically who have NTG, should be evaluated for nocturnal hypotension. Also, sleep apnea should be considered in such patients.¹⁸ In addition, it is worth having a conversation with the patient’s cardiologist or primary care doctor to determine whether aggressive hypertensive therapy is necessary and to recommend that these medications are not taken at bedtime.

OTHER FACTORS

Glaucoma is an optic neuropathy that has long been associated with pressure. IOP is an indication of what the pressure might be across the optic nerve head and one of two components responsible for the translaminar pressure difference.

Although ocular hypertension is associated with the development and progression of glaucoma, it is not necessarily causative of glaucoma, and there is a large group of ocular hypertensive patients who never develop glaucoma.

Therefore, clearly, other factors are at play in determining glaucoma risk and disease progression. One important factor is OPP. Patients who have low or widely fluctuating OPP are at higher risk of glaucoma development as well as progression, particularly in the NTG patient subgroup.¹⁵

ACTION STEP

So, what can we do with the information provided above to help our glaucoma patients?

Unfortunately, no device is approved for measuring OPP at this time. Thus, the best we can do for our glaucoma patients presently is to measure BP and calculate OPP using the formula mentioned above.

In fact, as more is learned about OPP, optometrists should consider readying themselves to implement some form of regular BP monitoring of their patients in an office setting. This is particularly important for patients who have NTG and have shown disease progression or in patients who are known to be on aggressive hypertensive medications. OM

Special thanks to Michael Cymbor, O.D., F.A.A.O., for reviewing this article.

REFERENCES

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DR. KRESCH is the owner of Michigan Contact Lens in the Detroit Metropolitan area and clinical assistant professor of Ophthalmology, Wayne State University School of Medicine. She has served as an optometrist in the glaucoma department of Columbia University Medical Center and New York Presbyterian Hospital. Dr. Kresch can be reached at info@michigancontactlens.com.