Papilledema as the Initial Presenting Clinical Sign of Subdural Hemorrhage

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Guor Wang, MD Papilledema as the Initial Presenting Clinical Sign of Subdural Hemorrhage Sunil Bellur, MD, Julie Thomasian, BS, Alex Hacopian, MD, Nancy Vilar, MD, PhD S ubdural hemorrhage (SDH) in adults classically presents with neurologic signs, such as gait disturbance, hemiparesis, altered consciousness, or cognitive deficits. Ophthalmic findings such as anisocoria, homonymous hemianopsia, cranial nerve palsies, and optic nerve edema can be seen in SDH but are rarely the initial presenting clinical sign (1,2). These ophthalmic signs are commonly due to increased intracranial pressure or direct compression of the optical pathway. Although the presence of optic nerve edema is rare in acute SDH, it is more prevalent in subacute and chronic SDH (1). Here, we report a rare case of a 24-yearold man presenting with papilledema as the initial clinical sign of a large subacute right-sided subdural hematoma. A 24-year-old man presented to the triage clinic with a 2-day history of a “red floater” in his right eye accompanied with pressure-type right ocular pain worse in the supine position and with extraocular movements. He also reported a 2-week history of new headaches with photophobia diagnosed as migraines and managed with naproxen and sumatriptan. His medical history includes refractive error and color vision deficiency. The patient is a recreational boxer with his last sparring session occurring 6 months before presentation. On initial examination, best-corrected visual acuity (BCVA) was 20/20 (Snellen chart) in both eyes, Ishihara color plates were 1/14 in both eyes, and intraocular pressure was 11 mm Hg in the right eye and 12 mm Hg in the left eye. Pupil examination was normal with no anisocoria or afferent pupillary defect, and extraocular movements were normal. Confrontational visual fields were full with no constriction. Dilated fundus examination revealed grade 2+ optic nerve edema in both eyes (Fig. 1) with a flame-shaped hemorrhage superiorly off the disc in the right eye. The remainder of the fundus examination was unremarkable. Optical coherence tomography (OCT) of the optic nerve head (ONH) confirmed nerve head elevation in both eyes. Department of Ophthalmology, George Washington University, Washington, District of Columbia. The authors report no conflicts of interest. Address correspondence to Sunil Bellur, MD, Department of Ophthalmology, George Washington University, 2150 Pennsylvania Avenue NW, Suite 2A, Washington, DC 20037; E-mail: sbellur@mfa. gwu.edu. e154 The patient was referred for neuroimaging given his history of possible head trauma from boxing, positional headaches, and bilateral optic nerve edema. MRI of the brain without contrast revealed a large right frontoparietal subdural hematoma in the subacute phase with 1.4 cm left midline shift, right sulcal effacement, and trapping of the posterior left lateral ventricle with early hydrocephalus and subfalcine herniation (Fig. 2). Urgent burr-hole evacuation of the hematoma was performed with successful evacuation of blood products. Repeat CT of the head without contrast showed re-expansion of brain parenchyma, and the patient achieved rapid recovery with no residual neurologic deficits; he was discharged home on postoperative day 4. On follow-up, the patient noted significant improvement in his headache and near resolution of his visual floaters. He denied any other visual or neurologic symptoms. Follow-up examination revealed BCVA 20/25 in both eyes with improvement of optic nerve head edema on fundus examination and OCT ONH. Visual fields were normal on automated visual field 30-2. This report shows a rare case of a large subdural hemorrhage in a young boxer without focal neurological deficits who presented with papilledema as his initial clinical sign. Although anisocoria is the most common ophthalmic finding in SDH, its prevalence decreases with chronicity while optic nerve edema’s prevalence increases (1,2). Vision loss from SDH is more commonly due to affliction to the posterior visual pathway with possible mechanisms including infarction of the occipital lobe and compression of the posterior cerebral artery due to transtentorial herniation (3). Optic neuropathy from prechiasmal injury is more rare— proposed mechanisms include vascular compromise of the optic nerve due to intracranial pressure exceeding perfusion pressure or parenchymal herniation causing direct compression of the anterior visual pathway (3,4). In this case, the patient’s papilledema was likely caused by boxing trauma leading to a chronic SDH and persistent increased intracranial pressure. Kushi et al (5) showed that SDH from boxing injuries are more likely to occur in younger patients, have longer lucid intervals, lack skull fractures or cerebral contusions, and involve trauma to the bridging and cortical veins; however, all patients in this study had acute SDH and initially presented with altered consciousness or headache. Bellur et al: J Neuro-Ophthalmol 2023; 43: e154-e155 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence FIG. 1. Bilateral color fundus photographs. Color fundus photograph demonstrates grade 2+ optic nerve edema in both eyes with flame-shaped hemorrhage off disc in the right eye. FIG. 2. MRI, coronal and axial views. T1 coronal and axial MRIs show a large right-sided subdural hemorrhage with midline shift. Our case is atypical in that the patient presented 6 months after the last sparring session and with visual symptoms as his predominant complaint. Given that SDH is an infrequent but potentially devastating cause of optic neuropathy and vision loss, findings of optic nerve edema in patients with remote trauma warrant neuroimaging. REFERENCES 1. Pevehouse BC, Bloom WH, McKissock W. Ophthalmologic aspects of diagnosis and localization of subdural hematoma. An Bellur et al: J Neuro-Ophthalmol 2023; 43: e154-e155 analysis of 389 cases and review of the literature. Neurology. 1960;10:1037. 2. Mitsumoto H, Conomy JP, Regula G. Ophthalmologic aspects of subdural hematoma. Cleve Clin Q. 1977;44:101–106. 3. Hollander DA, Stewart JM. Anterior pathway vision loss due to subdural haematoma. Br J Ophthalmol. 2003;87:1423–1424. 4. Kretz A, Preul C, Fricke HJ, Witte OW, Terborg C. Unilateral optic neuropathy following subdural hematoma: a case report. J Med Case Rep. 2010;4:19. 5. Kushi S, Saito T, Sakagami Y, Ohtsuki J, Tanjoh K. Acute subdural hematoma because of boxing. J Trauma. 2009;66:298–303. e155 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.