In-Flight G-Induced Retrobulbar Optic Neuropathy in a Fighter Pilot

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Gour Wang, MD In-Flight G-Induced Retrobulbar Optic Neuropathy in a Fighter Pilot Kenneth R. Taylor, MD, Yanjun Chen, MD, PhD S ince the days of the first flight surgeons, vision has been recognized as one of the most important assets of a pilot (1). Vision loss during flight can be catastrophic, often leading to controlled flight into terrain, loss of aircraft, and death of the pilot (2). Vision loss can be induced by highspeed turning maneuvers, which result in gravitational force along the craniocaudal vector, referred to as “G.” G-induced vision loss is transient, and vision returns in less than one second when the G-load is reduced (3). Our patient uniquely manifested a G-induced unilateral posterior ischemic optic neuropathy (PION) that later spontaneously resolved. An emergency flight line response was called for a 24year-old male US military student pilot for acute visual loss during a flight. The patient was flying the T-6 Texan II aircraft, a dual-seat fighter trainer aircraft used to train student pilots in the US Air Force, Navy, and Marine Corps (Fig. 1). Ten minutes before landing, the patient had engaged in a +5G (5 times the acceleration due to gravity) maneuver when he experienced a complete, sudden loss of vision in the right eye. He did not have confusion, loss of consciousness, or visual loss in the left eye. As per the patient’s report, complete visual field loss resolved to a right temporal defect within 6–9 seconds, and on landing a right temporal defect was confirmed on confrontation visual fields. The patient’s past ocular history was significant for a history of posterior vitreous detachment (PVD) and lattice degeneration in the right eye treated with laser photocoagulation (required by military aeromedical regulations) 6 months before. The patient was otherwise healthy. Review of systems was unremarkable apart from his vision loss, and the patient took no medications on a regular basis. Examination one hour later revealed a best-corrected visual acuity of 20/30 + 1 in the right eye and 20/25 in the left eye, a right relative afferent pupillary defect (RAPD), an intraocular pressure of 15 mm Hg in each eye, full extra- ocular motility, and a temporal visual field defect in the right eye alone. Slit-lamp examination and dilated fundus examination were unremarkable except for the aforementioned PVD and lattice degeneration with laser in the right eye. Ocular coherence tomography (OCT) of the retina and retinal nerve fiber layer (RNFL) thickness were unremarkable. Further evaluation by retina and neuro-ophthalmology included an MRI of the brain and orbit with and without contrast, an MRA of the head and neck, retinal fluorescein angiography and indocyanine green angiography, visual evoked potential, multifocal electroretinogram, carotid doppler, and cerebral angiogram. All testing was within normal limits. The patient was placed on a full dose aspirin on postevent day 1, which was discontinued at approximately day 60 with no additional intervention. The patient’s visual fields were monitored over an 86day follow-up, and the right temporal hemianopia progressively resolved (Fig. 2). An aeromedical waiver to resume flight duties was requested after resolution of the patient’s visual field defect, but the request was denied by headquarters. The patient was subsequently retrained to a different career field in the Air Force and had no recurrence of his visual symptoms. The patient’s presentation of, in particular, sudden onset of visual deterioration, the presence of optic nerve–related visual Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, Wisconsin. Supported in part by an unrestricted research grant from the Research to Prevent Blindness, Inc, to the Department of Ophthalmology and Visual Sciences at the University of Wisconsin. The authors report no conflicts of interest. Address correspondence to Kenneth R. Taylor, MD,Department of Ophthalmology and Visual Sciences, University of Wisconsin, 2880 University Avenue, Madison,WI 53705;E-mail:[e-mail] e172 FIG. 1. T-6 Texan II, the aircraft which the patient was flying during the maneuver that caused his vision loss, with the author (K.R.T.) pictured. Taylor and Chen: J Neuro-Ophthalmol 2021; 41: e172-e173 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence FIG. 2. Humphrey 30-2 visual fields at days 9, 18, 58, and 86 after the inciting event demonstrating progressive resolution of the patient’s visual field deficit. field defects, an RAPD, unremarkable ancillary studies (brain and orbital MRI and ocular vascular imaging), and lack of ocular findings that may explain his visual symptoms suggests PION as the mechanism for his visual loss (4,5). Although PION generally does not resolve and leaves the patient with optic atrophy that is visible on dilated fundus examination (4), our patient fortunately had spontaneous resolution of his visual symptoms and no documented optic atrophy on follow-up ophthalmoscopy. The OCT RNFL thickness was normal in the initial examination and not repeated in follow-up visits. Absence of OCT RNFL thinning in this patient is not unexpected as it takes weeks after the onset to develop RNFL thinning. The pathophysiologic processes contributing to PION include decreased perfusion pressure to the optic nerve and decreased venous outflow (4). Decreased optic nerve perfusion pressure occurs during high G flight as blood is pulled by gravitational force away from the cranium. Vision progressively narrows bilaterally to a central straw (greyout) and subsequently vanishes (blackout) (3). The G-strain maneuver, an exercise used in flight to prevent G-induced vision loss, involves muscular contraction of the lower extremities to prevent pooling of blood in the lower extremities and to maintain perfusion to the head and neck. However, under the stress of high G flight, novice pilots (such as our patient) often incorrectly contract the upper extremities and/or perform the Valsalva maneuver. An incorrectly performed G-strain increases venous outflow resistance in the head and neck. This combination of decreased arterial perfusion pressure due to G-force and increased venous outflow resistance seen with the Valsalva maneuver of an incorrectly performed G-strain creates a pathophysiologic environment where PION is significantly more likely to occur (4). Fortunately, despite the highly abnormal environment of high G flight, long-term vision loss associated with G-exposure is rare. Taylor and Chen: J Neuro-Ophthalmol 2021; 41: e172-e173 Although hypoperfusion and increased venous outflow pressure is one reason that PION could have occurred in this patient, the presence of a stretch injury to one or more of the collateral arterioles supplying perfusion to the optic nerve head is another possible mechanism for this retrobulbar optic neuropathy. A stretch injury could be seen to spontaneously resolve with recollateralization in approximately 90 days as was seen in this patient but is not commonly described as causative of PION. Transient compression by G-force in the craniocaudal vector is another possible etiology of this patient’s vision loss but could be seen as a hyperintense lesion on MRI orbits and is less likely. Regardless of mechanism, to the best of our knowledge, this is the first reported case in the literature of G-induced unilateral PION and of delayed spontaneous resolution. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: K. R. Taylor; b. Acquisition of data: K. R. Taylor; c. Analysis and interpretation of data: K. R. Taylor and Y. Chen. Category 2: a. Drafting the manuscript: K. R. Taylor and Y. Chen; b. Revising it for intellectual content: K. R. Taylor and Y. Chen. Category 3: a. Final approval of the completed manuscript: K. R. Taylor and Y. Chen. REFERENCES 1. Jones I. Flying Vistas: The Human Being as Seen Through the Eyes of the Flight Surgeon. Philadelphia, PA: J.B. Lippincott Company, 1937. 2. Church A. The science of avoidance. In: Air Force Magazine. Vol 99. Arlington, VA: Air Force Association, 2016:34–38. 3. Yilmaz U, Cetinguc M, Akin A. Visual symptoms and G-LOC in the operational environment and during centrifuge training of Turkish jet pilots. Aviat Space Environ Med. 1999;70:709–712. 4. Biousse V, Newman NJ. Ischemic optic neuropathies. N Engl J Med. 2015;372:2428–2436. 5. Hayreh SS. Posterior ischemic optic neuropathy: clinical features, pathogenesis, and management. Eye (Lond). 2004;18:1188–1206. e173 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.