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Alex S Huang,1 Anthony P Mai,2 Jeffrey L Goldberg,3 Thomas W Samuelson,4 William H Morgan,5 Leon Herndon,6 Tanner J Ferguson,2 Robert N Weinreb7 1Doheny Eye Institute, Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; 2Vance Thompson Vision, Sioux Falls, SD, USA; 3Byers Eye Institute, Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, USA; 4Minnesota Eye Consultants, University of Minnesota, Minneapolis, MN, USA; 5Lions Eye Institute, Centre for Ophthalmology and Visual Science, University of Western Australia, Perth, Western Australia, Australia; 6Department of Ophthalmology, Duke Eye Center, Duke University, Durham, NC, USA; 7Hamilton Glaucoma Center, Viterbi Family Department of Ophthalmology and Shiley Eye Institute, University of California San Diego, La Jolla, CA, USACorrespondence: Anthony P Mai, Email anthonymai.md@gmail.comAbstract: Nocturnal intraocular pressure (IOP) profiling has shown that the peak IOP usually occurs at night, particularly in patients with glaucoma. Multiple studies have demonstrated that these nocturnal IOP elevations drive glaucomatous progression, often despite stable daytime IOP. Existing vascular dysregulation and decreased nighttime blood pressure compound the damage via low ocular perfusion pressure while elevated nocturnal IOP disrupts axonal transport. These findings are consistent with studies that indicate lowering nocturnal IOP is important for slowing glaucoma progression. Many of the current treatment options lower nighttime IOP significantly less than daytime IOP. Non-invasive IOP-lowering treatments that effectively lower nocturnal IOP remain an unmet need in the treatment of glaucoma.Keywords: glaucoma, nocturnal intraocular pressure, translaminar pressure differential

A 76-year-old woman was referred to our hospital for evaluation of markedly high intraocular pressures (IOPs): ≥40 mmHg in both eyes. No intraocular inflammation, pseudoexfoliation, or glaucomatous optic neuropathy was observed on ophthalmological examination. The 24-hour IOP fluctuations, measured with a Goldmann tonometer in the sitting position at 8, 12, 16, 20, and 24 o' clock, were 22/17, 33/28, 41/33, 30/22, and 30/24 mmHg, respectively, and showed a peak in the afternoon. The patient was diagnosed with ocular hypertension, and microhook trabeculotomy (μLOT) (right eye with lens reconstruction, left eye initially pseudophakic) was performed. After μLOT surgery in both eyes (4 days postoperatively in the right eye and 1 day postoperatively in the left eye), IOP decreased in both eyes to 12/15, 11/14, 12/15, 10/11, and 10/10 mmHg, and the fluctuation range was suppressed. At 3 months postoperatively (measured at 8, 12, 16, 20, 24, and 4 o' clock), the effect was maintained at 14/15, 15/19, 14/19, 11/12, 13/14, and 13/13 mmHg, respectively, but was slightly attenuated. In a patient with marked 24-hour IOP fluctuation, μLOT was effective in reducing IOP values and fluctuation.

We describe the case of a primary open-angle glaucoma patient with re-elevated nocturnal sitting intraocular pressure (IOP) after restarting medical therapy due to a failing bleb. IOP was markedly higher than diurnal IOP during multiple-drug therapy in both eyes, but it did not increase in the left eye with a functional bleb without medical therapy after trabeculectomy with adjuvant mitomycin. However, nocturnal sitting IOP was re-elevated after restarting multiple-drug therapy due to a failing bleb, while diurnal IOP was maintained at a low level. [ABSTRACT FROM AUTHOR]