Prognosticators of Visual Acuity After Indirect Traumatic Optic Neuropathy

Background: The purpose of this study is to determine whether there are radiographic and systemic clinical characteristics that can predict final visual outcomes in patients with indirect traumatic optic neuropathy (iTON). Methods: This study is a retrospective, multicenter case series of adult patients with iTON treated initially at large, urban, and/or academic trauma centers with follow-up at an affiliated ophthalmology clinic. In addition to detailed cranial computed tomography characteristics, demographics, systemic comorbidities, coinjuries, blood products administered, and intracranial pressure, along with other factors, were gathered. LogMAR visual acuity (VA) at the initial presentation to the hospital and up to 12 months follow-up was collected. Results: Twenty patients met inclusion criteria; 16 (80%) were men with a mean age of 40.9 years (±20.9). Mean initial VA was 1.61 logMAR (∼20/800, ± 0.95), and final VA was 1.31 logMAR (∼20/400, ± 1.06). Three patients (4 eyes) had no light perception (NLP) VA at presentation and remained NLP at final follow-up. Of the predictors analyzed, only the initial VA was found to be a significant predictor of visual outcome. The presence of orbital fractures, intraconal and/or extraconal hemorrhage, as well as systemic comorbidities, were not found to significantly affect visual outcome. Conclusions: After evaluating multiple factors, initial VA was the only factor associated with visual prognosis in iTON. This knowledge may better enable clinicians to predict visual prognosis and set reasonable expectations with patients and families at the time of injury.

Original Contribution Section Editors: Clare Fraser, MD Susan Mollan, MD Prognosticators of Visual Acuity After Indirect Traumatic Optic Neuropathy Alex J. Wright, MD, Joanna H. Queen, MD, Emilio P. Supsupin, MD, Alice Z. Chuang, PhD, John J. Chen, MD, PhD, Rod Foroozan, MD, Ore-Ofe O. Adesina, MD Background: The purpose of this study is to determine whether there are radiographic and systemic clinical characteristics that can predict final visual outcomes in patients with indirect traumatic optic neuropathy (iTON). Methods: This study is a retrospective, multicenter case series of adult patients with iTON treated initially at large, urban, and/or academic trauma centers with follow-up at an affiliated ophthalmology clinic. In addition to detailed cranial computed tomography characteristics, demographics, systemic comorbidities, coinjuries, blood products administered, and intracranial pressure, along with other factors, were gathered. LogMAR visual acuity (VA) at the initial presentation to the hospital and up to 12 months follow-up was collected. Results: Twenty patients met inclusion criteria; 16 (80%) were men with a mean age of 40.9 years (±20.9). Mean initial VA was 1.61 logMAR (w20/800, ± 0.95), and final VA was 1.31 logMAR (w20/400, ± 1.06). Three patients (4 eyes) had no light perception (NLP) VA at presentation and remained NLP at final follow-up. Of the predictors analyzed, only the initial VA was found to be a significant predictor of visual outcome. The presence of orbital fractures, intraconal and/or extraconal hemorrhage, as well as systemic comorbidities, were not found to significantly affect visual outcome. Ruiz Department of Ophthalmology and Visual Science (AJW, JHQ, AZC, OOA), McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth), Houston, Texas; Robert Cizik Eye Clinic (AJW, JHQ, OOA), Houston, Texas; Lyndon B. Johnson Hospital (AJW, JHQ, OOA), Harris Health, Houston, Texas; Department of Diagnostic & Interventional Imaging McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth) (EPS), Houston, Texas; Departments of Ophthalmology and Neurology (JJC), Mayo Clinic, Rochester, Minnesota; Cullen Eye Institute (RF), Department of Ophthalmology, Baylor College of Medicine, Houston Texas; and Department of Neurology (OOA), McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth), Houston, Texas. Supported by National Eye Institute Vision Core Grant P30EY028102 and Research to Prevent Blindness. The authors report no conflicts of interest. Address correspondence to Ore-Ofe O. Adesina, MD, Robert Cizik Eye Clinic, 6400 Fannin Street, Suite 1800, Houston, TX 77030; E-mail: [e-mail] Wright et al: J Neuro-Ophthalmol 2022; 42: 203-207 Conclusions: After evaluating multiple factors, initial VA was the only factor associated with visual prognosis in iTON. This knowledge may better enable clinicians to predict visual prognosis and set reasonable expectations with patients and families at the time of injury. Journal of Neuro-Ophthalmology 2022;42:203–207 doi: 10.1097/WNO.0000000000001521 © 2022 by North American Neuro-Ophthalmology Society T raumatic optic neuropathy (TON) is a well-known cause of vision loss that occurs in approximately 2%–5% of patients with orbital injuries (1–3). Direct TON results from penetration or contusion of the optic nerve by a foreign body or from nerve impingement by fragments of the optic canal or boney skull base (2). The indirect mechanism of TON, however, is less well understood. It is speculated to result from blunt force transmission to the optic canal, where the optic nerve is tethered to the bone via its dural sheath. Forces transmitted through the calvarium result in damage to the nerve from direct axonal injury and/or shearing of the vasa vasorum, with subsequent edema, ischemia, and potentially necrosis of the optic nerve (4–6). Regardless of mechanism, TON is a clinical diagnosis made with evidence of optic nerve damage, including decreased visual acuity (VA), color vision, and contrast sensitivity, afferent pupillary defect, and visual field loss (6,7). Previous reports show that patients with direct TON experience poor initial visual acuities and limited improvement, which is expected as damage results from direct compression/severing of the optic nerve, causing irreversible axonal damage (2,8). Visual outcomes are almost universally poor, and patient counseling with respect to visual prognosis is relatively straightforward. Contrastingly, patients with indirect TON (iTON) have more variable visual prognoses, ranging from 20/20 to no light perception (NLP), with stable VA taking 3–6 months to reach (1). Counseling at 203 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution time of injury consists primarily of a “wait-and-see” approach that can be frustrating for patients (9). Treatment options are relatively limited for patients with iTON, further compounding patient frustration. There is no Level-1 evidence that steroids provide a definitive benefit, and surgical options have also failed to show definite benefit. There are concerns over survival implications in patients with traumatic brain injury and low Glasgow coma scale scores (10). Most notably, the International Optic Nerve Trauma study demonstrated that optic canal decompression did not show improved visual outcomes with steroids (11). Although described previously (12,13), factors underlying the variability in visual outcomes in iTON patients have not been robustly studied. Trauma with force sufficient to cause iTON often causes collateral ocular trauma in addition to systemic injuries. In prior studies, the most common comorbid injuries in iTON patients were orbital and facial fractures (70%) (14). Radiological findings in trauma patients associated with a higher incidence of iTON included orbital fractures, intra- and extraconal hemorrhage, intraconal emphysema, and periorbital soft tissue/eyelid injury (15–17). However, comorbid systemic conditions, including metabolic or cardiovascular disease, blood volume loss at time of trauma, and sepsis during hospitalization, have not been well studied in association with iTON. The purpose of our study was to determine radiographic and systemic clinical characteristics affecting final visual outcomes in iTON patients. This knowledge may better enable clinicians to predict visual prognosis and set reasonable expectations with patients at the time of injury. METHODS This retrospective case series was conducted in patients diagnosed with unilateral or bilateral iTON at time of initial ophthalmology consult at the Memorial Hermann Hospital Texas Medical Center (MHH TMC) in Houston, TX, the Baylor St. Luke’s Medical Center in Houston, TX, and the Mayo Clinic in Rochester, MN, between January 1, 2011 and March 1, 2015. Adult patients with iTON were initially treated at large, urban, and/or academic trauma centers with follow-up at an affiliated ophthalmology clinic. Institutional Review Board (IRB) approvals were obtained from the Committee for the Protection of Human Subjects at The University of Texas Health Science Center, Baylor College of Medicine, Mayo Clinic, and Memorial Hermann Health System. All research adhered to the tenets of the Declaration of Helsinki and was HIPAA compliant. The IRBs determined that informed consent could be waived. Patients were identified using ICD-9 diagnosis code for optic nerve injury (950.0). Patients who had evidence of optic nerve dysfunction, defined as visual field loss, color vision deficits, optic atrophy/pallor, and/or an afferent pupillary defect, were reviewed. Patients must have been 204 18 years or older at time of initial trauma with a computed tomography (CT) maxillofacial region or orbits obtained during initial hospitalization, showing no evidence of direct optic nerve injury. VA must have been tested at time of initial consult or within 7 days of initial injury. Patients with at least 3 months of follow-up after initial injury, with VA measured at time of examinations, were included; up to 12 months of follow-up data were recorded. Patients were excluded if they had trauma-related globe injuries, including corneal or scleral laceration, corneal abrasion, vitreous hemorrhage, commotio retinae, traumatic retinal detachment, hyphema, or cataract, choroidal rupture, and/or optic nerve avulsion. Patients with preexisting optic nerve disorders, significant media opacities, or retinal diseases were excluded. No patients had prior baseline eye exams because they presented acutely with trauma to the emergency department. Data collected included demographics (age at initial eye examination, sex, race/ethnicity), initial injury characteristics and comorbidities (mechanism of trauma, hemoglobin levels, blood products given, and Systemic Inflammatory Response Syndrome [SIRS] criteria, sepsis criteria, or septic shock criteria met at any point during hospitalization), and pretrauma systemic comorbidities. Administration of steroids during hospitalization was also recorded. Ocular examination results, including VA and presence of soft tissue injury, were recorded at the time of initial evaluation and for each follow-up visit. An MHH TMC neuroradiologist (EPS), masked to clinical history, reviewed CT images obtained during hospitalization for presence of orbital fractures, optic canal fractures, intra- and extraconal hemorrhage and emphysema, and intracranial hemorrhage and edema. VA was measured using a Snellen chart and converted to logMAR by 2log10(VA), with the following adjustments: count fingers was coded as 20/1,500 (logMAR of 1.8), hand motion as 20/4,000 (logMAR of 2.3), light perception as 20/8,000 (logMAR of 2.6), and NLP as 20/20,000 (logMAR of 3). VA change was calculated by subtracting initial VA (in logMAR) from final VA (in logMAR). Data were summarized by mean and SD for continuous variables and frequency (%) for discrete variables. The paired t test was used to compare VA changes at initial and final visits. Stepwise regression analysis was performed to identify prognostic factors associated with final VA and change in VA. All statistical analyses were performed using SAS for Windows version 9.4 (Cary, NC). P value of less than 0.05 was considered to be statistically significant. RESULTS Twenty-two eyes of 20 patients were included. The mean age was 40.9 years (±20.9). Sixteen patients (80%) were male, and 9 (45%) were white. Nine patients originally identified as meeting inclusion criteria were subsequently Wright et al: J Neuro-Ophthalmol 2022; 42: 203-207 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Demographics, presenting medical characteristics, and treatment of 20 patients with indirect traumatic optic neuropathy Variable Summary Statistics (20 Patients) Demographics Age [years, mean (±SD)] Gender (male, %) Race (%) White Black Hispanic Other Mechanism of injury Motor vehicle collision (%) Industrial accident (%) Assault (%) Blunt (%) Others (fall, gunshot wound, sports, (%)) Preexisting systemic disease Diabetes mellitus (%) Hypertension (%) Cardiovascular disease (%) Renal disease (%) Laboratory values and systemic diagnosis Initial hemoglobin [g/dL, mean (±SD)] Initial hematocrit [%, mean (±SD)] SIRS (%) Sepsis (%) Septic shock criteria met (%) Treatment Blood products given (%) Vasopressors used (%) High-dose steroids administered in admission (%) ICP bolt placed (%) 40.9 (±20.9) 16 (80%) 9 5 4 2 (45%) (25%) (20%) (10%) 8 4 3 2 3 (40%) (20%) (15%) (10%) (15%) 1 (5%) 5 (25%) 2 (10%) 0 (0%) 13.19 (±1.75) 39.03 (±5.26) 6 (30%) 3 (15%) 1 (5%) 4 2 2 3 (30%) (10%) (10%) (15%) ICP, intracranial pressure; SIRS, systemic inflammatory response syndrome. excluded after closer review of the CT images identified optic canal fractures. Motor vehicle accidents were the most frequent mechanism of injury (8 [40%]), followed by industrial accidents (4 [20%]) and assault (3 [15%]) (Table 1). Five patients (25%) had hypertension, and 2 had (10%) cardiovascular disease. Initial mean hemoglobin and hematocrit levels were 13.19 g/dL (±1.75) and 39.03% (±5.26), respectively. Six patients (30%) met SIRS criteria. Four patients (30%) received blood products, 2 (10%) received vasopressors, 2 (10%) received high-dose steroids, and 3 (15%) had intracranial pressure monitors placed (Table 1). Nineteen eyes (86%) presented with periorbital soft tissue injury. Eighteen patients (82%) had anterior orbital wall fractures, with 14 (64%) exhibiting posterior orbital wall fractures on CT imaging. Five (25%) also had LeForte fractures. Eight patients (36%) had intraconal hemorrhages, and 12 (55%) had extraconal hemorrhages. Only 2 patients (12%) required cantholysis (Table 2). Mean initial recorded VA was 1.61 logMAR (w20/800, ± 0.95). Final recorded VA was 1.31 logMAR (w20/400, ± 1.06), an improvement of 20.30 log MAR (Snellen equivWright et al: J Neuro-Ophthalmol 2022; 42: 203-207 alent of 3 lines, ± 0.49), which was significantly better compared with baseline (P = 0.010). All 4 NLP eyes (3 patients) at presentation remained NLP at the final visit. Of 18 eyes with VA better than NLP at presentation, 11 (61%) had VA improvement by 2 or more lines, and 7 (39%) remained the same. Final VA for non-NLP eyes was associated with initial VA (P = 0.005). For every 1 logMAR increase in initial VA, final VA increased (worsened) by 0.60 logMAR (±0.19). No other injury characteristics or treatments were correlated with final VA. No factors were associated with a change in VA for non-NLP eyes. CONCLUSIONS We found that final VA was significantly correlated with initial VA (P , 0.001). Other studies have found a similar trend in ocular trauma outside of TON. The Ocular Trauma Classification Group looked at more than 2,500 eye injuries to develop the Ocular Trauma Score and showed that presenting VA was the most important predictor of final visual outcome (18). Similarly, the International Optic Nerve 205 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 2. Summary of presenting ocular and head injury characteristics Ocular Injury Characteristics Periorbital soft tissue injury (%) Eyelid laceration (%) Cantholysis performed (%)* Intraconal hemorrhage (%) Extraconal hemorrhage (%) Intraconal emphysema (%) Extraconal emphysema (%) Anterior orbital wall fracture (%) Posterior orbital wall fracture (%) Head injury characteristics Intracranial hemorrhage (%)† Intracerebral edema (%)‡ Anterior clinoid fracture (%) LeFort fracture (%) Other skull/facial fracture (%)§ N = 22 Eyes 19 (86%) 9 (41%) 2 (12%) 8 (36%) 12 (55%) 3 (14%) 11 (50%) 18 (82%) 14 (64%) N = 20 patients 8 (47%) 2 (13%) 0 (0%) 5 (25%) 15 (79%) *Missing 5 data points from Baylor St. Luke’s Medical Center site. † Missing 3 data points. ‡ Missing 4 data points. § Missing 1 data point. Study Group study evaluating the effect of surgery vs steroids vs observation only found presenting VA to be predictive of final visual outcome (19). In a review by Carta et al, poor prognostic factors included loss of consciousness and lack of visual recovery after 48 hours (12). In a review by Homes and Sires, absence of visually evoked potentials also portended a poorer visual outcome (20). While interpretation of results from the International Optic Nerve Study Group was limited without standardization of CT technique/grading, the study showed that specific CT findings were not found to affect visual outcomes (19). After a standardized review of CT scans, including fractures, soft tissue trauma, orbital hemorrhage, and orbital emphysema, our study also found that no comorbid injury was predictive of or associated with final VA. Although our imaging findings are associated with a higher incidence of iTON, any combination of their presence or severity was not found to be predictive of final VA. This is likely due to the variable manner in which blunt force is applied during trauma and how that force is distributed as it propagates through the periocular tissue to the optic nerve. The increased incidence of orbital fractures with iTON is likely reflective of the overall severity and amount of force received in the trauma but does not appear to be predictive of the amount of force that the nerve itself is subjected to in the orbit or optic canal nor its impact on vision. Mechanism of injury was also not found to be associated with final visual outcomes in our study, reemphasizing the variability of traumatic mechanisms associated with iTON. In prior studies, iTON patients have been more commonly male and younger than 50 years (7), similar to our cohort. Comorbid systemic conditions, including blood volume loss at time of trauma, requirement for intracranial pressure monitor206 ing, and development of sepsis during hospitalization, did not show an increased risk of poorer visual outcomes in our cohort. Presence of preexisting conditions, such as metabolic or cardiovascular disease, was also not predictive of visual outcomes. These results may suggest that secondary stresses on the body from systemic disease, either inflammatory or ischemic, do not compound optic nerve damage from iTON or affect final visual outcomes when managed appropriately. It also highlights that extensive workup or review of laboratory evaluation is not required from an ophthalmic standpoint, as it is not necessary for visual prognostication. An important observation made in our study is that an additional 9 patients were excluded after further review of CT imaging showed previously missed fractures of the optic canal, recategorizing the injury mechanism as direct TON. This highlights the importance of careful imaging review to help delineate between direct and indirect TON because this may change patient counseling. It also points to the possibility of iTON being incorrectly overdiagnosed. In our study, CT was favored over MRI because it is readily available for the assessment of acute trauma patients in the emergency setting, is a faster scan for patients with polytrauma, and provides superior demonstration of bony injuries. This makes it a more valuable tool for the classification of direct and indirect TON, which can be useful to help educate patients regarding visual prognosis between the 2 entities. MRI changes to the optic nerve after iTON have been documented and include hyperintensity of the nerve seen on diffusion-weighted imaging in the acute setting (21) and reduction of fractional isometropy in diffusion tensor imaging, which may be related to axonal degeneration over time (21). This latter imaging modality requires at least 2 weeks for changes to be seen and is not widely available for use at all trauma centers. While MRI evaluation of iTON may be an area of future investigation, at this stage, the clinical application of MRI, with its limitations in the acute trauma setting, was not our standard of practice. While the majority of our patients did not receive therapeutic intervention for their iTON, potential therapies, such as optic canal decompression, intravenous steroids, and erythropoietin (EPO), have been investigated for iTON in the acute setting (10,11,22). Surgical decompression of the optic canal, intravenous steroids, and observation, when compared in a prospective multicenter trial, were not significantly different when corrected for baseline vision (19). Iatrogenic effects of steroid treatment must also be considered; the CRASH study found that patients treated with megadose intravenous methylprednisolone for acute traumatic brain injury were at an increased risk of death and disability at 6 months of follow-up, leading to the early termination of the study (23). With regards to EPO, the Traumatic Optic Neuropathy Treatment Trial compared treatment with EPO, steroids, and observation. While color vision was significantly improved in the EPO group, the best-corrected VA of all 3 groups improved significantly, with no statistically significant Wright et al: J Neuro-Ophthalmol 2022; 42: 203-207 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution difference identified among them with regards to this outcome measure (22). In a recent large review of interventions for iTON by Wladis et al for the American Academy of Ophthalmology, there was no clear evidence that any 1 treatment, including optic canal decompression, steroids, EPO, or carbidopa-levodopa, improves outcomes in these patients (24). Given the available literature, none of the patients in our study were felt to be candidates for intervention; however, further analysis of these treatments, particularly EPO, in this patient population is worthy of more investigation. A weakness of this study is the small number of patients who met inclusion criteria. Therefore, factors that may have had a small effect on final visual outcomes could have been missed. The small sample is in part due to the stringent criteria required to isolate VA changes secondary to the indirect trauma alone, as well as the relative rarity of this diagnosis. Expanding the number of centers and enrollment period is a possible way to increase sample size. Finally, it is assumed that injury to the optic nerves in our patient cohort was from force applied directly to the nerves in the orbit and optic canal at time of injury and not from compressive optic neuropathy from elevated intraorbital pressures from orbital hemorrhages or edema. While 55% of eyes did have associated orbital hemorrhages, only 2 required cantholysis, presumably from a tight orbit and elevated intraocular pressure. In all cases, the primary cause of optic neuropathy was determined to be iTON. Poor presenting VA is associated with a poorer visual prognosis in patients with iTON. Comorbid injuries and systemic conditions do not appear to affect visual outcomes. Careful review of the appropriate imaging is important to help correctly differentiate direct and indirect TON, as visual outcomes overall tend to be worse in the former. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: O.-O. Adesina; b. Acquisition of data: J. Queen, E. Supsupin; c. Analysis and interpretation of data: O.-O. Adesina, A. Wright, J. Queen, A. Chuang, J. Chen, R. Foroozan, E. Supsupin; Category 2: a. Drafting the manuscript: A. Wright, O.-O. Adesina, J. Queen, A. Chuang, J. Chen, R. Foroozan, E. Supsupin; b. Revising it for intellectual content: A. Wright, O.-O. Adesina, J. Queen, J. Chen, R. Foroozan, E. Supsupin, A. Chuang; Category 3: a. Final approval of the completed manuscript: A. Wright, J. Queen, E. Supsupin, A. Chuang, J. Chen, R. Foroozan, O.-O. Adesina. REFERENCES 1. Lessell S. Indirect optic nerve trauma. Arch Ophthalmol. 1989;107:382–386. 2. Magarakis M, Mundinger GS, Kelamis JA, Dorafshar AH, Bojovic B, Rodriguez ED. Ocular injury, visual impairment, and blindness associated with facial fractures: a systematic literature review. Plast Reconstr Surg. 2012;129:227–233. 3. Cook T. Ocular and periocular injuries from orbital fractures. 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