UNILATERAL PAPILLEDEMA: MEDICAL MANAGEMENT AND TREATMENT

Date

2013-04-12

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Nguyen, Tran

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Purpose: Introduction: Papilledema, also known as optic disc swelling, occurs in the setting of increased intracranial pressure. The etiology of papilledema may be due to several causes, and medical management varies depending on the etiology. Therefore, diagnostic testing is important in determining the source of elevated intracranial pressure. While headache is a common manifestation of papilledema, visual obscuration is most notable and frightful event for the patient. Medical management of papilledema requires serial clinical evaluation and serial visual acuity measurements, fundoscopic examination and visual field testing in order to monitor the efficacy of treatment. Methods: Single patient chart review Results: Case Description: A 30 year-old Caucasian female presents to the Emergency Department with chief complaints of acute vision loss in her right eye and periorbital headache. Physical exam was within normal limits. Brain MRI revealed right optic nerve enhancement. Patient was admitted for optic neuritis workup and received IV steroids. She was discharged after four days with a Medrol dose pack and clinic follow up. At her follow up visit at ophthalmology clinic, her vision improved slightly but she complained some of her visual field remains dark. Visual exam revealed 20/40 (OD), 20/30 (OS), 8 mm pupil OU, 2+ afferent papillary defect OD, and visual field showed inferior scotoma. Clinical differential diagnosis included idiopathic intracranial hypertension (IIH) versus optic neuritis based on neuroimaging and patient's body habitus. Patient started on corticosteroid treatment and taper, and clinician order lumbar puncture. On follow up visit 3 weeks later, patient continue to complain of visual loss OD. Visual field test revealed shifted visual defect relative to initial test. Results of lumbar puncture showed CSF opening pressure within normal limits when adjusted for patient's body habitus. Optic neuritis CSF workup revealed negative oligoclonal bands. IIH ruled out due to unilateral papilledema and normal CSF opening pressure. A working diagnosis of an independent optic neuritis was made. Patient started IV steroids, oral steroid taper, and follow up visit in 4 weeks. Conclusions: Discussion: This case is an example of optic neuritis manifestation prior to clinical and laboratory findings of Multiple Sclerosis. The case also illustrates the importance of serial clinic evaluations and neuroimaging aid in determining the etiology of papilledema.

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