Nonarteritic Anterior Ischemic Optic Neuropathy as a Complication of Air Travel: A Case Report

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Guor Wang, MD Nonarteritic Anterior Ischemic Optic Neuropathy as a Complication of Air Travel: A Case Report Soha S. Noorani, BS, Daniel S. Kermany, BS, Mohammad Pakravan, MD, MBA, Chaow Charoenkijkajorn, MD, Andrew G. Lee, MD A nterior ischemic optic neuropathy (AION) is the most common cause of acute unilateral visual loss with optic disc edema in older adults. It is divided into arteritic AION (AAION), from giant cell arteritis, and nonarteritic (NAION). Many risk factors have been proposed in association with NAION, including hypertension, diabetes mellitus, hypercholesterolemia, obstructive sleep apnea, tobacco usage, ischemic heart disease, and more. However, the precise mechanism for pathogenesis may be multifactorial (1). Commercial air travel requires changes in cabin pressure for oxygenation at higher altitudes, which may precipitate dehydration and transient hypercoagulability leading to venous thrombosis. NAION has been reported after commercial and military flights (2,3). We describe a case of NAION associated with both deep vein thrombosis (DVT) and intracranial ischemia after commercial air flight. To our knowledge, this is the first such report in the English-language ophthalmic literature. A 74-year-old Hispanic woman developed acute painless vision loss in the left eye (left eye) within hours following commercial air travel. Her ocular history was significant for acute painless vision loss to counting fingers level with a relative afferent pupillary defect (RAPD) and optic disc edema in the right eye (right eye) 4 months earlier. Ultimately, this resolved to stable optic atrophy in the right eye, consistent with NAION in the right eye. Her medical history was significant for hypertension, degenerative osteoarthritis, depression, migraines, and osteoporosis. Her prior hepatocellular carcinoma and uterine Philadelphia College of Osteopathic Medicine (SN), Suwanee, Georgia; Department of Ophthalmology (DK, MP, CC, AGL), Blanton Eye Institute, Houston Methodist Hospital, Houston, Texas; Departments of Ophthalmology, Neurology, and Neurosurgery (AGL), Weill Cornell Medicine, New York, New York; Department of Ophthalmology (AGL), University of Texas Medical Branch, Galveston, Texas; University of Texas MD Anderson Cancer Center (AGL), Houston, Texas; Texas A and M College of Medicine (DK, AGL), Bryan, Texas; and Department of Ophthalmology (AGL), The University of Iowa Hospitals and Clinics, Iowa City, Iowa. The authors report no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the full text and PDF versions of this article on the journal’s Web site (www. jneuro-ophthalmology.com). Address correspondence to Andrew G. Lee, MD, Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital, 6560 Fannin Street, Ste 450, Houston, TX 77030; E-mail: aglee@ houstonmethodist.org e68 cancer were in remission. She had a Type-B carotid cavernous fistula obliterated with endovascular embolization. Surgical and procedural history included appendectomy, bunionectomy, Cesarean section, hysterectomy, and colonoscopy. Family history was notable for hypertension, diabetes mellitus, and myocardial infarction. The patient denied alcohol, tobacco, or other illicit drug use. Her medications and supplements included aspirin, omeprazole, quetiapine, simvastatin, lisinopril, lorazepam, triamcinolone, vitamin C, magnesium, and omega-3 fatty acids. Prior to flying, she was advised to avoid in-flight alcohol consumption or dehydration and to consider compression stockings. She was already taking 81 mg of aspirin daily. The patient traveled on a 3-hour flight from Houston, TX to El Salvador, subsequently developing acute visual loss on arrival. She denied symptoms of jaw claudication, headache, or scalp tenderness. The patient had no other neurologic symptoms or signs. Three days following her flight, she was hospitalized and had markedly elevated blood pressure. Treatment involved intravenous steroids, and she returned to Houston Methodist Hospital 1 month later for workup. Magnetic resonance imaging (MRI) of the head and orbits showed no enhancement of the optic nerve. MRA of the head did not have evidence of recurrent or residual carotid cavernous fistula. Ultrasound of the lower extremities revealed a DVT in the right gastrocnemius vein. Electrocardiogram was normal. Echocardiogram did not identify a cardiogenic embolic source or patent foramen ovale. Laboratory studies detected a low hemoglobin value of 9.9 g per deciliter (normal, 12–15.5 g/dL). Further laboratory testing values, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), were within expected values (See Supplemental Digital Content 1, Table 1, http://links.lww.com/WNO/A592). Neuro-ophthalmic examination identified count fingers vision at 4 feet in the right eye and 20/80 in the left eye. Ishihara color plates were 0/14 in the right eye and 1/14 in the left eye. As noted previously, RAPD was present in the right eye. Intraocular pressure was normal in both eyes. Slit lamp biomicroscopy, motility, and external examinations were normal. Fundus examination showed optic disc atrophy in the right eye and optic disc-edema in the left eye (Fig. 1A, B). Initial optical coherence tomography (OCT) showed thinning in the retinal nerve fiber layer (RNFL) with global values of 53 mm in the right eye and RNFL thickening of 229 mm in Noorani et al: J Neuro-Ophthalmol 2024; 44: e68-e69 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence the left eye (Supplemental Digital Content). The optic disc edema resolved to optic atrophy in the left eye, and repeat OCT had global RNFL values of 60 mm in the right eye and 85 mm in the left eye (Supplemental Digital Content 2, http://links.lww.com/WNO/A593). Follow-up MRI 3 months after the flight detected a potential acute infarct (Fig. 2A) and microvascular chronic ischemic disease within the white matter (Fig. 2B). NAION is a common and well-recognized cause of acute vision loss in older adults, typically following vascular insufficiency. Systemic vasculopathies like hypertension and diabetes are commonly implicated in typical NAION (1), although thromboembolic cases of NAION are atypical and rare. There are at least 2 reported cases of NAION following air travel, including in pilots (2,3). The 2 cited mechanisms for NAION here have been thromboembolism (originating from a deep venous source) and hypoxia from decreased cabin pressure (2). Interestingly, our patient had both intracranial ischemia and a DVT while presenting with NAION in the left eye. Commercial air flights pressurize passenger cabins to altitudes ranging from 6,000 to 8,000 feet above sea level (3). At higher altitudes, the partial pressure of oxygen (O2) decreases, impacting the O2 saturation of hemoglobin in the blood. A drop in available O2 reduces hemoglobin’s affinity for oxygen, allowing quicker release to tissues, causing a corresponding right shift on the oxygen–hemoglobin dissociation curve (4). In healthy individuals, the difference between cabin pressure and pressure at sea level generally produces no ischemic symptoms. However, healthy individuals could develop DVT, so patients with predisposing risk factors are often advised on potential countermeasures for venous thromboembolism (VTE). In one systematic review, the rate of clinical VTE following prolonged travel was 0.05% for symptomatic DVT (5). Asymptomatic VTE, however, may be more common. Graduated compression stockings reduced travel-related VTE, but aspirin did not; low-molecular-weight heparin (LMWH) trended toward efficacy in one study but remains controversial (5). Regardless of VTE risk, all air travelers should avoid dehydration and exercise leg muscles frequently (5). Patients without VTE risk factors flying for less than 6 hours may not need DVT prophylaxis, but travelers with 1 or more vasculopathic risk factors should consider compression stockings and/ FIG. 2. A. Image shows a tiny focus of diffusion-weighted image hyperintense signal located in superior ventral pons concerning for a tiny acute infarct. B. Generalized atrophy of the brain parenchyma. T2 image. Nonspecific hyperintensities in the white matter likely represent chronic microvascular ischemic disease, along with slight ventriculomegaly likely associated with volume loss centrally. or LMWH for flights exceeding 6 hours (5). Our patient had nonmodifiable risk factors, including previous NAION in the right eye and prior malignancy, as well as chronic anemia. In summary, NAION is a common cause of acute optic neuropathy in adults. Air travel predisposes individuals to states of hypoxia and hypercoagulability. These mechanisms for NAION are not seen in typical NAION but suggest a unique pathogenic mechanism related to air travel. Patients with multiple risk factors—especially prior NAION—should consider maximizing control of treatable vasculopathies along with in-flight countermeasures to reduce the risk of VTE. STATEMENT OF AUTHORSHIP Conception and design: S. Noorani, M. Pakravan, C. Charoenkijkajorn, A. G. Lee; Acquisition of data: S. S. Noorani, D. S. Kermany, M. Pakravan, C. Charoenkijkajorn, A. G. Lee; Analysis and interpretation of data: S. Noorani, M. Pakravan, C. Charoenkijkajorn, A. G. Lee; Drafting the manuscript: S. Noorani, M. Pakravan, C. Charoenkijkajorn, A. G. Lee; Revising the manuscript for intellectual content: S. Noorani, Daniel Kermany, M. Pakravan, C. Charoenkijkajorn, A. G. Lee; Final approval of the completed manuscript: S. Noorani, Daniel Kermany, M. Pakravan, C. Charoenkijkajorn, A. G. Lee. REFERENCES FIG. 1. A. Optic disc edema in the left eye. B. Optic disc atrophy in the right eye more pronounced inferiorly. Noorani et al: J Neuro-Ophthalmol 2024; 44: e68-e69 1. 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