Bilateral Optic Nerve Enhancement in Posterior Ischemic Optic Neuropathy Secondary to Hypovolemic Shock

A 63-years-old diabetic man was admitted to the emergency department after he was found lethargic at home. On admission, he had a systolic blood pressure of 55 mm Hg and a blood sugar of 638 mg/dL.

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Guor Wang, MD Bilateral Optic Nerve Enhancement in Posterior Ischemic Optic Neuropathy Secondary to Hypovolemic Shock Mehdi Tavakoli, MD, Michael S. Vaphides, DO A 63-years-old diabetic man was admitted to the emergency department after he was found lethargic at home. On admission, he had a systolic blood pressure of 55 mm Hg and a blood sugar of 638 mg/dL. He was diagnosed with hypovolemic shock due to diabetic ketoacidosis and underwent treatment, including intubation and respiratory support at the intensive care unit. After 3 weeks, when his mental status improved and he was extubated, he reported bilateral no light perception (NLP). Ophthalmologic examinations confirmed bilateral NLP vision and fixed dilated pupils with mild optic nerve pallor in both eyes. The patient denied pain and other temporal arteritis symptoms, and the erythrocyte sedimentation rate was 6 mm/h. Fat-suppressed contrast-enhanced orbital MRI revealed bilateral enhancement of the intraorbital and intracanalicular portions of the optic nerve and its sheath. No restricted diffusion was noted (Fig. 1). He received 1 g of intravenous methylprednisolone for 3 consecutive days with no improvement of the vision. The cerebrospinal fluid study showed normal cell count and negative cytology. Other inflammatory and infectious investigations, including Lyme, tuberculosis, syphilis, HIV, sarcoidosis, antiaquaporin, and anti-myelin oligodendrocyte glycoprotein antibodies, were all negative. A temporal artery biopsy was also unremarkable. The enhancement of the optic nerves persisted and became more pronounced on the second 12-week follow-up MRI (Fig. 2). The constellation of findings was consistent with bilateral posterior ischemic optic neuropathy (PION). We report a rare case of bilateral optic nerve enhancement in hypotension-related PION. To the best of our knowledge, this is the third reported case of PION with bilateral optic nerve enhancement because of hypotension. The senior author reported the first case in 2004 (1), and Finelli (2) reported the second case in 2018. Three features shared by all cases include bilateral enhancement, visual acuity of NLP, and the persistent optic nerve enhancement in follow-up MRI weeks later. Although contrast enhancement of the optic nerve is a radiologic hallmark of the optic nerve inflammations including demyelinating optic neuritis, enhancement of the optic nerve Ophthalmology Department, Capital and Coast District Health Board, Wellington, New Zealand. The authors report no conflicts of interest. Address correspondence to Mehdi Tavakoli, MD, 1720 University Boulevard, Birmingham, AL 35233; E-mail: mehditavakoli@uabmc. edu Tavakoli and Vaphides: J Neuro-Ophthalmol 2022; 42: e577-e578 or its sheath is also occasionally noted in patients with arteritic ischemic optic neuropathy (ION) and nonarteritic anterior ION (NA-AION) (3,4). Rizzo et al have reported but not demonstrated the enhancement in 2 out of 32 patients with NA-AION (4). Adesnia et al (5) compared the optic nerve enhancement in NA-AION vs optic neuritis and showed the former group had a specific pattern of optic disc enhancement without diffusion-weighted imaging signal. They postulated that preferential shunting of blood flow to the ischemic portions of the optic disc can explain the optic disc enhancement. The central portion of the optic nerve is perfused by the peripheral centripetal vascular system formed by the pial vascular plexus from the ophthalmic artery with vulnerability FIG. 1. Postcontrast T1 fat-suppressed axial (A) and coronal (B, C) orbital MRI showed enhancement of the optic nerves and sheaths 3 weeks after presentation. Diffusionweighted image (D) and apparent diffusion coefficient scan (E) are unremarkable. e577 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence In summary, the orbital MRI enhancement of the optic nerves after hypotensive PION is rare, persistent over weeks, and associated with a very poor visual acuity. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: M. Tavakoli and M. S. Vaphiades; b. Acquisition of data: M. S. Tavakoli; c. Analysis and interpretation of data: M. Tavakoli and M. S. Vaphiades. Category 2: a. Drafting the manuscript: M. Tavakoli and M. S. Vaphiades; b. Revising it for intellectual content: M. Tavakoli and M. S. Vaphiades. Category 3: a. Final approval of the completed manuscript: M. Tavakoli and M. S. Vaphiades. REFERENCES FIG. 2. Postcontrast T1 fat-suppressed axial (A) and coronal (B, C) orbital MRI show persistent and more pronounced contrast enhancement of the optic nerves 12 weeks after presentation. to low perfusion (6). Although in the arteritic ischemic optic neuropathy, the inflamed vascular walls compromise the blood–brain barrier; in the case of PION, ischemia may interrupt this barrier causing contrast enhancement within the optic nerve. We think that the severity of the ischemic damage may contribute not only to the poor visual outcomes but also to the extensive interruption of the blood–brain barrier that persistently enhances the optic nerve. Persistent enhancement of the optic nerve is a well-described radiologic feature of radiation-induced optic neuropathy and attributed to the persistence of endothelial cell proliferation, hyalinization, and thrombosis of blood vessels (7). The mechanism of this phenomenon in PION is not clear. e578 1. Vaphiades MS. 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