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Show Photo Essay Rapidly Sequential Vision Loss From Posterior Ischemic Optic Neuropathy Due to Methicillin-Susceptible Staphylococcus Aureus Bacteremia Sultan S. Aldrees, MD, MSc, Jonathan A. Micieli, MD, CM FIG. 1. MRI revealing acute ischemic changes in the intracanalicular optic nerves as demonstrated by hyperintensity on diffusion-weighted imaging (A) and corresponding low signal on apparent diffusion coefficient images (B). Abstract: A 63-year-old man with a history of high-grade bladder cancer was admitted to the intensive care unit (ICU) with renal failure and methicillin-susceptible Staphylococcus aureus bacteremia originating from his nephrostomy tube. While in the ICU, he had painless, severe loss of vision in the right eye followed by his left eye 12 hours later. Visual acuity was no light perception in each eye. He was anemic, and before each eye lost vision, there was a significant decrease in blood pressure. Dilated fundus examination was normal, and MRI showed hyperintense signal in the bilateral intracanalicular optic nerves on diffusion-weighted imaging and a corresponding low signal on apparent diffusion coefficient imaging. He was diagnosed with bilateral posterior ischemic optic neuropathies (PION), and despite transfusion and improvement in his systemic health, his vision did not recover. PION may be seen in the context of sepsis, and patients with unilateral vision loss have a window Department of Ophthalmology and Vision Sciences (SSA, JAM), University of Toronto, Toronto, Canada; Department of Ophthalmology (SSA), King Saud University, Riyadh, Saudi Arabia; Division of Neurology (JAM), Department of Medicine, University of Toronto, Toronto, Canada; Kensington Vision and Research Centre (JAM), Toronto, Canada; and Department of Ophthalmology (JAM), St. Michael's Hospital, Toronto, Canada. The authors report no conflicts of interest. Address correspondence to Jonathan A. Micieli, Kensington Vision and Research Centre, 340 College Street, Suite 501, Toronto, ON M5T 3A9, Canada; E-mail: jmicieli@kensingtonhealth.org 420 for optimization of risk factors if a prompt diagnosis ismade. Journal of Neuro-Ophthalmology 2020;40:420-422 doi: 10.1097/WNO.0000000000000850 © 2019 by North American Neuro-Ophthalmology Society A 63-year-old man was admitted to the intensive care unit (ICU) after he presented to the hospital with malaise and decreased oral intake. He had a medical history of high-grade bladder cancer diagnosed 1 year earlier and treated with transurethral removal of bladder tumor and chemotherapy. He subsequently developed renal failure from recurrence of the cancer, and a nephrostomy tube was placed. In the ICU, he was found to have worsening renal function (creatinine 1,032 mmol/L) and methicillin-susceptible Staphylococcus aureus (MSSA) bacteremia originating from the nephrostomy tube. He was treated with intravenous vancomycin and pipercillintazobactam. During his stay in the ICU, he developed sudden, painless vision loss in the right eye and was found to have a visual acuity of no light perception. His left eye subsequently lost vision 12 hours later also with no light perception. His pupils were sluggishly reactive to light, and dilated fundus examination revealed normal-appearing optic nerves and retinae. He was found Aldrees and Micieli: J Neuro-Ophthalmol 2020; 40: 420-422 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo Essay to be anemic (hemoglobin 82 g/L) and hypotensive. His blood pressure decreased to 69/49 and 70/45 immediately before vision loss in the right and left eyes, respectively. MRI of the brain and orbits showed hyperintense signal in the bilateral intracanalicular optic nerves on diffusion-weighted imaging (DWI) and a corresponding low signal on apparent diffusion coefficient (ADC) imaging (Fig. 1). There were no other orbital or brain abnormalities. Despite transfusion with 2 units of packed red blood cells and the use of norepinephrine, his vision did not recover. His creatinine improved with the treatment of sepsis. At a follow-up neuro-ophthalmology visit 3 months later, his vision remained no light perception in both eyes, and there was optic disc pallor in both eyes (Fig. 2). The sudden painless vision loss in both eyes with sluggishly reactive pupils and a normal dilated fundus examination localized the process to the posterior optic nerves and a clinical diagnosis of PION. MRI of the brain and orbits was performed and confirmed the diagnosis of PION with restricted diffusion in the intracanalicular portions of both optic nerves (hyperintense DWI with a corresponding low ADC signal). The mechanism was likely a result of his anemia and profound hypotension in the context of MSSA bacteremia and renal failure. Norepinephrine was used as a last resort to try and elevate the blood pressure, given that he had no light perception vision, and there was no effect with blood transfusion. However, vasopressor drugs may exacerbate the ischemia of the optic nerve by causing vasoconstriction of terminal arterioles, and an association between prolonged use of vasopressors and inotropic agents and PION has been reported (1,2). PION is believed to be a multifactorial process with male sex, obesity, anesthesia duration, blood loss, and colloid as a percent of nonblood replacement identified as risk factors from a case-control study using the American Society of Anesthesiologists Postoperative Visual Loss Registry (3). In most cases of perioperative PION, hypotension and anemia are believed to be the most important risk factors (4). These risk factors were also present in this case of MSSA-related sepsis, and the reduced perfusion to the posterior optic nerves resulted in severe, irreversible vision loss. PION has been reported in the context of sepsis related to necrotizing fasciitis (5), septic shock related to aspiration pneumonia (6), dengue fever (7), and perforated sigmoid diverticulitis (8). These 4 cases represented 3 women and 1 man with a mean age of 55 years (range 42-65). All cases of vision loss were preceded by various degrees of hypotension and anemia, and one patient had a brief pulseless electrical activity and required large volume administration and multiple vasopressor infusions (8). The initial visual acuity at diagnosis was no light perception in all eyes at presentation, and there was no improvement in vision after a mean follow-up time of 194 days (range 42 days to 15 months). All patients had normal-appearing optic nerves at presentation, whereas one case had associated bilateral central retinal artery occlusions and bilateral optic disc edema, in additional to optic nerve involvement seen on DWI and ADC MRI sequences (6). Unlike the previous cases reported in the literature, this patient had MSSA bacteremia, rapidly sequential vision loss with a clear interval between vision loss in both eyes and remained alert and oriented throughout the process. The time interval between involvement of the second eye offered a window for rapid optimization of risk factors. Unfortunately his second eye lost vision before this was considered. Treatment with steroids or other modalities such as hyperbaric oxygen was not administered, given his systemic infection and the lack of evidence for their efficacy. Although his systemic health improved, he continued to have bilateral no light perception vision. Sepsis should be considered a risk factor for PION, and FIG. 2. Optic disc 3 months after vision loss demonstrating bilateral optic nerve atrophy. Aldrees and Micieli: J Neuro-Ophthalmol 2020; 40: 420-422 421 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo Essay prompt recognition may lead to improved outcomes in unilateral cases. STATEMENT OF AUTHORSHIP Category 1: a) Conception and design: S. S. Aldrees and J. A. Micieli; b) Acquisition of data: S. S. Aldrees and J. A. Micieli; c) Analysis and interpretation of data: S. S. Aldrees and J. A. Micieli. Category 2: a) Drafting the manuscript: S. Aldrees and J. A. Micieli; b) Revising it for intellectual content: S. S. Aldrees and J. A. Micieli. Category 3: a) Final approval of the completed manuscript: S. S. Aldrees and J. A. Micieli. REFERENCES 1. Shapira OM, Kimmel WA, Lindsey PS, Shahian DM. Anterior ischemic optic neuropathy after open heart operations. Ann Thorac Surg. 1996;61:660-666. 422 2. Lee LA, Lam AM. Unilateral blindness after prone lumbar spine surgery. Anesthesiology. 2001;95:793-795. 3. The Postoperative Visual Loss Study Group. Risk factors associated with ischemic optic neuropathy after spinal fusion surgery. Anesthesiology. 2012;116:15-24. 4. Sadda SR, Nee M, Miller NR, Biousse V, Newman NJ, Kouzis A. Clinical spectrum of posterior ischemic optic neuropathy. Am J Ophthalmol. 2001;132:743-750. 5. Haas LE, van der Ploeg RS, Quak JJ, Otten M. A young man with severe and disabling complications of septic shock. Am J Crit Care. 2015;24:450-452. 6. Gui W, Frisen ET, Bonelli L, Wang YE, Arnold AC. Severe bilateral optic nerve and retinal hypoperfusion in a patient with acute respiratory distress syndrome and septic shock. Am J Ophthalmol Case Rep. 2017;6:84-87. 7. Hughes EH, Graham EM, Wyncoll DLA. Hypotension and anaemia-a blinding complication. Anaesth Intensive Care. 2007;35:773-775. 8. Lee LA, Nathens AB, Sires BS, McMurray MK, Lam AM. Blindness in the intensive care unit: possible role for vasopressors. Anesth Analg. 2005;100:192-195. Aldrees and Micieli: J Neuro-Ophthalmol 2020; 40: 420-422 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |