EyeWorld Asia-Pacific September 2015 Issue

47 EWAP GLAUCOMA September 2015 Views from Asia-Pacific Ivan GOLDBERG, MD Clinical Associate Professor & Head, Glaucoma Unit University of Sydney & the Sydney Eye Hospital c/o Eye Associates, 187 Macquarie Street, Sydney NSW 2000 Australia Tel. no. +61-2-9247-9972 Fax no. +61-2-9337-5557 eyegoldberg@gmail.com F ascination with the role of intraocular pressure in the initiation and progression of glaucoma damage continues to grow. While it is no longer considered the essence of the disease group and no longer forms part of the de nition of the condition, along with increasing age and a positive family history, IOP levels have been con rmed as a major risk factor. Reduction in IOP provides a patient’s visual safety margin. But what is important? Mean IOP? Peak IOP? The IOP area under the curve? With our current very limited sampling, we do not know. By providing a clue as to an eye’s peak diurnal IOP, the water drinking provocative test (WDT) may help unravel some of these mysteries; it will be continuous IOP monitoring that will provide de nitive answers. As if these questions were not challenging enough, we remain ignorant about the effects on optic nerve head health of the interplay between IOP and blood pressure (which determines the ocular perfusion pressure) and between IOP and intracranial pressure (which determines the translaminar pressure). Imbalance in both these parameters has been shown to be important in both the onset and progression of glaucoma damage. How might these concepts contribute to patient outcomes? We need to remain aware of IOP variability to make repeated measurements and to of provocative tests such as the WDT judiciously, in the context of a patient’s central corneal thickness (as a surrogate for corneal hysteresis) and drainage angle con guration. We need to familiarize ourselves with a patient’s co-morbidities and their concomitant medications, such as systemic hypertension and its treatment, to look for low blood pressures, especially during sleep, when IOP increases from the horizontal position. These are parameters we can measure and modify to improve outcomes. While vitally important in glaucoma management, IOP is but one of three pressures at the optic nerve head pressure crossroads. Its modi cation is a partial solution to the challenge of protecting patients from glaucoma disability. Editors’ note: Prof. Goldberg has no relevant nancial interests. Naris Kitnarong, MD, MBA Associate Professor in Ophthalmology Department of Ophthalmology, Faculty of Medicine Siriraj Hospital, Mahidol University 2 Prannok, Bangkok, Thailand 10700 Tel. no. +66-24198033 Fax no. +66-24111906 naris.kit@mahidol.ac.th I n clinical practice, treating glaucoma always focuses on IOP as a major manipulated factor. However, even though IOP is considered the most important factor for glaucoma diagnosis and progression, one should keep in mind that IOP is not everything in glaucoma. IOP as well as other clinical evaluation parameters such as optic disc and visual elds should be used together. Individual patients must have individual target IOPs. We should not be satis ed if IOP alone is below target because IOP is not just a number. In patients with progressive eld loss despite good IOP control or patients with high risk of progression, the occasional IOP measurement during of ce hours may not be suf cient. We should consider other aspects of IOP which may play roles in progression such as short- and long-term IOP uctuation, IOP rise at night, during sleep and in supine position, and factors affecting IOP measurement. Understanding other factors besides IOP such as ocular blood ow, OPP, and ICP may account for disease progression in some patients. Finally, glaucoma management cannot be completed if we check only IOP. We need to completely consider all aspect of IOP as well as other factors affecting the optic nerve head. Editors’ note: Dr. Kitnarong has no nancial interests related to his comments behavior is most responsible for glaucoma progression? Mean IOP? Peak IOP? In truth, we don’t know, largely because we have such a low sampling rate for IOP assessment. We are limited to measuring IOP only a few times a year, and only during office hours on weekdays, in the sitting position. Home tonometry is coming into practice and will very likely provide insight into the patterns of IOP that are most likely to lead to progression. But perhaps not. IOP is undoubtedly important. How, though, do we explain the patients with high IOP who never progress, or the patients with low IOP who go blind from glaucoma? Perhaps IOP’s relevance is relative to other intertwined factors, such as blood pressure or intracranial pressure. Ocular perfusion pressure Ocular perfusion pressure (OPP) is the difference between systemic blood pressure and IOP. OPP is reduced in situations where IOP is high and/or blood pressure is low. Both of these often happen simultaneously at night. When OPP is low, the eye is relatively less well perfused, and the optic nerve (and other ocular structures) are at risk of ischemic injury. “A plethora of studies support that low OPP is a risk factor for the development of glaucoma,” said Alon Harris, MS, PhD, Indiana University School of Medicine, Bloomington. Among patients with low OPP, those who are being treated with systemic anti- hypertensive therapy are more at risk than those who are not on such therapy. “Perhaps these patients have larger nocturnal blood pressure dips associated with their therapy, or maybe their autoregulatory mechanism are impaired,” Dr. Harris said. Interest in OPP’s role in the glaucoma disease process is growing. “OPP could be incorporated into glaucoma management as a risk factor or as a therapeutic target. But first we need to better understand the complex relationship between blood pressure, IOP, and glaucoma,” Dr. Harris said. Intracranial pressure The potential role of intracranial pressure (ICP) in the glaucoma process is easy to conceptualize. “The intraocular space and the intracranial space are 2 fluid-filled compartments separated by the lamina cribrosa,” said Rand Allingham, MD , Duke University, Durham, NC. If we continued on page 53