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Figure 1. This slit lamp image shows a trace of both corneal edema and cells in the anterior chamber and a few keratic precipitates on the patient’s left corneal endothelium. She also presented with an IOP of 40 mm Hg in this eye. Can you identify the cause of her blurred vision and pain?
A 27-year-old female awoke with a very slight pain and blurred vision in her left eye. Although there was no redness, she was troubled by the blurred vision and presented to the emergency department, from where she was referred to the eye clinic. She had no history of medical issues and never wore corrective lenses.
Her presenting uncorrected visual acuities were 20/25 OD (correctable to 20/20) and 20/40 OS (correctable to 20/25). Although her right eye’s pupil was equal, round, and reactive to light and accommodation, her left pupil was slow to react to light, and slightly dilated. Her intraocular pressures (IOP) measured 16 mm Hg OD and 40 mm Hg OS.
Upon slit lamp evaluation, a trace of both corneal edema and cells in the anterior chamber (AC) were found, and a few keratic precipitates were visible on her left eye’s corneal endothelium (Figure 1). The right eye’s cornea was clear. Her angles were both open, the vitreous was clear, and no cells were seen in vitreous of either eye with a bright slit beam. The direct undilated ophthalmoscopic exam was normal in both eyes. By the third day, her IOP returned to normal range and her AC and cornea was clear after 1 week.
She was asked to return in 1 month for refraction and dilated exam and instructed to call immediately if any symptoms returned.
The patient presented with an acute case of significantly elevated IOP and signs of nongranulomatous anterior chamber inflammation without any conjunctival injection, as would be expected in an anterior uveitis.1 This is a classic presentation of glaucomatocyclitic crisis, also known...
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The patient presented with an acute case of significantly elevated IOP and signs of nongranulomatous anterior chamber inflammation without any conjunctival injection, as would be expected in an anterior uveitis.1 This is a classic presentation of glaucomatocyclitic crisis, also known as Posner-Schlossman syndrome (PSS).2
This inflammatory glaucoma was originally described in 1948 as a cyclitic, self-limiting, and benign condition that usually occurs in individuals between the third and sixth decade of life.1,3 Recent information however reveals that PSS patients carry an increased risk of primary open angle glaucoma and need to be regularly monitored throughout the rest of their lives.3
PSS will cause trabeculitis due to the accumulation of inflammatory elements in the intertrabecular spaces.4 A study from 1995 tested DNA samples collected during attacks of 3 patients with PSS.5 Researchers extracted and tested the aqueous DNA of these patients and compared them with the aqueous DNA of 10 patients without PSS undergoing cataract extraction. All 3 specimens were positive for amplified genomic fragments of herpes simplex virus and negative for varicella zoster virus and cytomegalovirus.4 This implies a possible viral role in the condition’s development and may explain the cyclical nature in some patients with PSS, as herpes viruses are typically latent within the nervous system. Some of my patients have had several events. One of my most memorable patients, now age 45, has had attacks twice a year for the past 12 years.
The literature offers 2 suggested treatments for patients who have multiple attacks of PSS. 1) Prolonged oral antiviral treatment and 2) trabeculectomy with anti-metabolite treatment has been reported to be successful, if the oral antiviral treatment fails.1,6 Both of these are now rarely advised. Today, surgeons may prefer less invasive procedures, such as minimally invasive glaucoma surgeries (MIGS).
This patient’s left eye was treated with timolol 0.50% dosed once a day (in the morning) for 3 days, prednisolone forte 1% every 4 hours, and then tapered down for the next week. She was reminded to call ASAP if similar symptoms occurred, and have yearly eye examinations.
Matthew Garston, OD, is an adjunct professor at the New England College of Optometry and was a senior staff optometrist in the medical department at MIT for 43 years.
References
1. Wang L, Yin G, et al. Posner-Schlossman syndrome: a 10 year review of clinical experience. Annals of Eye Science. 2017;2(7):51. doi:10.21037/aes.2017.05.02
2. Posner A, Schlossman A. Syndrome of unilateral recurrent attacks of glaucoma with cyclitic symptoms. Arch Ophthal. 1948;(39)4:517-535. doi:10.1001/archopht.1948.00900020525007
3. Jap A, Sivakumar M, Chee S. Is the Posner-Schlossman syndrome benign? Ophthalmol. 2001;108(5):913-918. doi:10.1016/s0161-6420(01)00551-6
4. Bodh S, Kumar V, Raina U, Ghosh B, Thakar M. Inflammatory glaucoma. Oman J Ophthalmol. 2011;4(1):3-9. doi:10.4103/0974-620X.776555.
5. Yamamoto S, Pavan-Langston D, Tada R, et al. Possible role of herpes simplex virus in the origin of Posner- Schlossman syndrome. Am J Ophthalmol. 1995;19(6):796-8. doi:10.1016/S0002-9394(14)72788-6
6. Sobolewska B, Deuter C, Doycheva D, Zierhut M. Long term oral therapy with valganciclovir in patients with Posner-Schlossman syndrome. Graefes Arch Clin Exp Ophthalmol. 2014;252(1):117-124.
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