| OCR Text |
Show PHOTO ESSAY Regression of Bilateral Optic Disc Edema After Discontinuation of Amiodarone Roman Shinder, MD, Larry P. Frohman, MD, and Roger E. Turbin, MD, FACS • II] At Presentation : i ] 2 Months Later 15 Months Later FIG. 1. Serial fundus photographs show gradual resolution of bilateral optic disc edema after discontinuation of amiodarone. Abstract: A 54- year- old non- obese woman treated with amiodarone reported blurred vision and had bilateral optic disc edema with relative preservation of visual function. Neurologic examination, brain imaging, and lumbar puncture opening pressures were normal, effectively ruling out increased intracranial pressure. Amiodarone was discontinued and the optic disc edema completely resolved over 15 months. In the absence of alternative explanations for the optic disc findings, amiodarone toxicity is suggested. (/ Neuro- Ophthalmol 2006; 26: 192- 194) A 54- year- old woman with no ocular history reported the recent onset of blurred vision and floaters in the right eye without headaches. She had begun amiodarone 600 mg per day 6 months earlier for atrial fibrillation in the setting of myocardial infarction and had required a pacemaker and placement of a mechanical valve for mitral valve stenosis 8 months earlier. The patient's other medications included warfarin and Zolpidem. Her height was 5 feet 5 inches and she weighed 150 lbs. General physical and neurologic examination was normal without heart failure or cor pulmonale. Visual acuity was 20/ 15 in both eyes and Ishihara color vision testing was normal. The pupils were equal in size, briskly reactive to light, and without afferent defect. Slit lamp examination were normal with the exception of mild corneal verticillata. Funduscopic examination showed bilateral optic disc edema ( Fig. 1) confirmed on optical coherence tomography ( OCT) ( Fig. 2). Automated static perimetry revealed visual fields with mild blind spot enlargement and minimal peripheral constriction in both eyes ( Fig. 3). Department of Ophthalmology, UMDNJ- NJMS, Newark, New Jersey. Supported by the Research to Prevent Blindness, Inc., New York, NY; Fund for the New Jersey Blind, Newark, NJ; Lions Eye Research Foundation of New Jersey, Newark, NJ; The Eye Institute of New Jersey, Newark, NJ; and the Gene C. Coppa Memorial Fund, Newark, New Jersey Address correspondence to Roger E. Turbin, MD, FACS, UMDNJ-NJMS, Department of Ophthalmology, 90 Bergen St., Room 6177, Newark, NJ 07103; E- mail: turbinre@ umdnj. edu 192 J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 Optic Disc Edema in a Patient Treated with Amiodarone J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 0 20 40 60 80 100 120 140 160 180 200 220 240 0 20 40 60 80 100 120 140 160 180 200 220 240 TEMP SUP NAS N= TEMP TEMP SIP NAS If IB* At Presentation 0 20 40 60 80 100 120 140 160 180 200 220 240 TEW SUP NAS WF TEMP 0 20 40 60 80 100 120 140 160 180 200 220 240 TEMP SUP NAS If BP 0 20 40 60 80 100 120 140 160 180 200 220 240 TEMP SUP NAS tf TEMP TEM> 8 Months Later Microns Microns 300 110nm i i i i i i i i i i i 0 20 40 60 80 100 120 140 160 160 200 220 240 SUP NAS NF TEMF 0 20 40 60 80 100 120 140 160 180 200 220 240 TEMP SUP NAS INF TEMP 0 20 40 60 TEMP SUP 100 120 140 160 180 200 220 240 NAS INF TEMP 15 Months Later FIG. 2. Optical coherence tomography ( OCT) of the right and left optic nerves at presentation shows optic disc edema with the plane of the image through the horizontal nasotemporal axis. OCT scans show gradual resolution of nerve fiber layer thickening over 15 months. ( The black line represents the tomographic plot of the actual nerve fiber layer elevation plotted against age- matched normals [ in green] and abnormals [ red] at P < 0.05. The early scans show so much optic disc elevation that the plots are mostly off the upper end of the available scale.) 193 J Neuro- Ophthalmol, Vol. 26, No. 3, 2006 Shinder et al a^:=. j.=-.-. » = j=:..".-. •' : liiiipifii : IP: < & • • • • • • • • • • • • • • • m • •••• u a • • • a &. •••• &. » « ••• B B » si: FIG. 3. Automated static perimetry performed at presentation shows mildly enlarged blind spots and mild constriction in both fields. A high- resolution CT scan of the head and orbits with contrast was normal. The presence of a pacemaker prevented MR scanning. A lumbar puncture performed at presentation and repeated 2.5 months into her course revealed normal opening pressures of 160 mm and 150 mm of water. Cerebrospinal fluid constituents, including cell count and cytology, were normal. The optic disc edema was attributed to amiodarone toxicity and this medication was promptly discontinued. Over the next 15 months, the optic disc edema gradually resolved as shown by serial optic disc photographs and OCT ( Figs. 1 and 2). Visual acuity and color vision testing remained normal throughout the course and visual fields showed continued improvement over the ensuing 7 months ( Fig. 4). This patient developed bilateral optic disc edema without substantial visual loss mimicking papilledema. However, investigation for increased intracranial pressure was negative. Because we could discover no alternative explanation, we blamed the ophthalmic findings on amiodarone toxicity. Although cited as occurring in up to 1% to 2% of patients taking the medication ( 1), the true incidence of amiodarone optic neuropathy and the mechanism by which the drug causes optic neuropathy are incompletely characterized. Furthermore, the visual complaints in patients with amiodarone optic neuropathy may be insidious or difficult to distinguish from other forms of optic neuropathy I0TBL DEVIATION s e. FIG. 4. Automated static perimetry performed 8 months after discontinuation of amiodarone therapy shows regression of blind spot enlargement and constriction. affecting a similar patient population with cardiovascular risk factors. Chronicity, bilateral presentation, and progression over several months favor drug toxicity. The clinical severity of this drug- related optic neuropathy has been characterized as milder than that described in anterior ischemic optic neuropathy, and patients may have preserved visual function ( 2,3). The optic disc swelling is typically bilateral and symmetric and can be quite marked ( 4). Visual field defects may be mild and reversible or severe and permanent ( 5). Optic disc swelling usually resolves many months after discontinuation of amiodarone ( 6,7), as occurred in our patient. REFERENCES 1. Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol 1999; 127: 610- 2. 2. Feiner LA, Younge BR, Kazmier FJ, et al. Optic neuropathy and amiodarone therapy. Mayo Clin Proc 1987; 62: 702- 17. 3. Gittinger JW Jr, Asdourian GK. Papillopathy caused by amiodarone. Arch Ophthalmol 1987; 105: 349- 51. 4. Nazarian SM, Jay WM. Bilateral optic neuropathy associated with amiodarone therapy. J Clin Neuroophthalmol 1988; 8: 25- 8. 5. Mantyjarvi M, Tuppurainen K, Ikaheimo K. Ocular side effects of amiodarone. Surv Ophthalmol 1998; 42: 360- 6. 6. Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter [ Editorial]. J Neuroophthalmol 2005; 25: 232- 6. 7. Nagra PK, Foroozan R, Savino PJ, et al. Amiodarone induced optic neuropathy. Br J Ophthalmol 2003; 87: 420- 2. 194 © 2006 Lippincott Williams & Wilkins |
