Journal français d’ophtalmologie (2014) 37, 231—236
Disponible en ligne sur
ScienceDirect www.sciencedirect.com
SFO COMMUNICATION
Two cases of bilateral amiodarone-associated optic neuropathy夽 À propos de deux cas de neuropathie bilatérale à l’amiodarone B. Chassang a, N. Bonnin a,∗,b, X. Moisset c, B. Citron d, P. Clavelou c, F. Chiambaretta a,b a
RMND-M2O Pole, Ophthalmology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France b EA 7281 R2D2, Biochemistery Laboratory, Medicine Faculty, Auvergne University, 63000 Clermont-Ferrand, France c RMND-M2O Pole, Neurology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France d Medical and Surgical Cardiology Pole, Cardiology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France Received 26 November 2013; accepted 9 December 2013 Available online 24 February 2014
KEYWORDS Amiodarone; Optic neuropathy; Iatrogenic disease; Papilledema
夽 ∗
Summary Introduction. — The widespread use of amiodarone is limited by its toxicity, notably to the optic nerve. We report two cases of bilateral optic nerve neuropathy due to amiodarone, and provide a detailed description of the disease. Observations. — The first case was a 59-year-old man complaining from insidious monocular loss of vision within ten months of initiating amiodarone. Funduscopy and optical coherence tomography showed bilateral optic disc edema. The second case was a 72-year-old man presenting with a decrease in visual acuity in his left eye for a month. Funduscopy showed a left optic nerve edema, and fluorescein angiography showed bilateral papillitis. In both cases, the clinical presentation was not suggestive of ischemic neuropathy, because of the preservation of visual acuity and the insidious onset. In addition, both cardiovascular and inflammatory work-up were normal. An amiodarone-associated neuropathy was suspected, and amiodarone was discontinued with the approval of the cardiologist, with complete regression of the papilledema and a stabilization of visual symptoms.
Oral communication presented at the 119th Congress of the French Society of Ophthalmology in May 2013. Corresponding author. E-mail address: [email protected] (N. Bonnin).
0181-5512/$ — see front matter © 2014 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.jfo.2013.12.004
232
B. Chassang et al. Discussion. — Differentiating between amiodarone-associated optic neuropathy and anterior ischemic optic neuropathy may be complicated by the cardiovascular background of such patients. The major criterion is the absence of a severe decrease in visual acuity; other criteria are the normality of cardiovascular and inflammatory work-up, and the improvement or the absence of worsening of symptoms after discontinuation of amiodarone. Conclusion. — Amiodarone-associated neuropathy remains a diagnosis of exclusion, and requires amiodarone discontinuation, which can only be done with the approval of a cardiologist, and sometimes requires replacement therapy. © 2014 Elsevier Masson SAS. All rights reserved.
MOTS CLÉS Amiodarone ; Neuropathie optique ; Iatrogénicité ; Œdème papillaire
Résumé Introduction. — L’amiodarone est l’anti-arythmique le plus répandu mais son utilisation est limitée par sa toxicité notamment au niveau du nerf optique. Nous rapportons deux cas de neuropathie bilatérale du nerf optique dus à l’amiodarone et à travers ces deux cas, nous apportons une description précise de la maladie. Observations. — Le premier cas est celui d’un homme de 59 ans se plaignant de baisse d’acuité visuelle insidieuse depuis dix mois après initiation d’un traitement par amiodarone. L’examen du fond d’œil montrait un œdème papillaire bilateral. Le second cas est celui d’un homme de 72 ans consultant pour une baisse d’acuité visuelle de l’œil gauche depuis un mois. L’examen du fond d’œil montrait un œdème papillaire gauche et l’angiographie à la fluorescéine confirmait l’existence d’une papillite bilatérale. Dans les deux cas, la présentation n’était pas évocatrice de neuropathie ischémique du fait de la presentation insidieuse et de la modeste baisse d’acuité visuelle. De plus, les bilans cardiovasculaires et inflammatoires étaient normaux. Une neuropathie iatrogène à l’amiodarone était suspectée et le traitement était stoppé après accord du cardiologue. Une régression de l’œdème papillaire était observée ainsi qu’une stabilisation des symptômes visuels. Discussion. — Différencier une neuropathie optique à l’amiodarone d’une neuropathie optique ischémique antérieure peut être complexe en raison des antécédents vasculaires de ces patients. Le principal critère est l’absence de baisse brutale de l’acuité visuelle; d’autres arguments tels que la normalité des bilans cardiovasculaires et inflammatoires, l’amélioration ou l’absence d’aggravation des symptômes après l’arrêt de l’amiodarone étayent le diagnostic. Conclusion. — La neuropathie iatrogène à l’amiodarone reste un diagnostic d’exclusion et impose l’arrêt d’amiodarone qui ne peut être fait qu’avec le consentement du cardiologue et nécessite parfois un traitement substitutif. © 2014 Elsevier Masson SAS. Tous droits réservés.
Introduction
Observations
Amiodarone has become a widely used class III antiarrhythmic drug. However, its use can be limited by serious toxicities and side effects, with almost 50% of long-term users resultantly discontinuing the drug [1]. Due to its lipophilic nature, amiodarone has strong tissue affinity, and its toxicity is ubiquitous, affecting the lungs, thyroid, skin, nervous system, liver, and eyes. There are a number of ocular adverse effects including corneal microdeposits, anterior subcapsular lens opacities, multiple chalazia, dry eye syndrome, halo vision and optic neuropathy [2]. Proper diagnosis of toxic optic neuropathy can justify drug withdrawal and hope of restored visual function. Every cardiologist must be aware of this potential adverse effect and ask their patients about visual symptoms.
Case 1 A 59-year-old man complained of non-painful insidious decreased vision, with a visual field defect in his right eye. This man had been undergoing amiodarone treatment (200 mg daily) for tachyarrhythmia for eleven months. He had a history of hypertension, dyslipidemia, cardiomyopathy and hyperuricemia. His medication included warfarin, bisoprolol, irbesartan, simvastatin, allopurinol and pantoprazol. Neurological examination was normal. The brain MRI was normal. Visual acuity was 20/25 in the right eye and 20/20 in the left eye. Funduscopy showed a bilateral optic disc swelling predominating on the left eye (Fig. 1). His pupils reacted equally with no relative afferent pupillary defect.
Two cases of bilateral amiodarone-associated optic neuropathy
Figure 1.
233
Retinophotographies of patient no 2. A and C. Right eye: lower-sectoral optic disc edema. B and D. Left eye: optic disc edema.
There was a central scotoma in the right visual field and an arciform scotoma in the left visual field (Fig. 2). Spectral domain optic coherency tomography (SD-OCT) showed a bilateral increase in optic nerve fiber thickness predominating on the left papilla (Fig. 3). SD-OCT is an optical signal acquisition and processing method that captures micrometer-resolution three-dimensional images from the retina. The peripapillary retina nerve fiber layer (RNFL) scan showed an increase in the left eye RNFL thickness that was above the 95th percentile of the normative data. The right eye RNFL thickness increase was sectoral, predominating on the lower quadrant. After discussion with the patient’s cardiologist, amiodarone was discontinued, and bisoprolol increased. After 3 months, the visual recovery was total,
in terms of both visual acuity and visual field, with no cardiac disturbances. Fundus examination had normalized. No relapse occurred after a four-year follow-up.
Case 2 A 72-year-old man, taking amiodarone (200 mg daily) for 8 months for atrial fibrillation, consulted our department for decreased vision in his left eye for 1 month. His medical history comprised a mantle cell lymphoma in remission, and arterial hypertension. His treatments were telmisartan and acenocoumarol. Visual acuity was measured at 20/20 in his right eye and 20/25 in his left eye. Slit lamp examination showed bilateral amiodarone corneal deposits, and
Figure 2. Kinetic perimetry of the patient no 1. Arciform scotoma in the left eye and central scotoma in the right eye, evocative of optic neuropathy.
234
B. Chassang et al.
Figure 3. Optical coherence tomography of patient no 1. Global increased left eye RNFL thickness (OS) and lower-sector increased right eye RNFL thickness (OD).
ocular pressure was normal. Fundus examination showed a papilledema in the left eye, and there was a doubt about the same aspect in the right eye (Fig. 4). Kinetic campimetry showed a significant bilateral narrowing with no special systematization (Fig. 5). Fluorescein angiogram showed a bilateral dye leakage in both optic nerves, confirming bilateral papillitis (Fig. 4). Cardiological and inflammatory assessment and brain imaging were performed, and were normal. An amiodarone-associated neuropathy was suspected, so amiodarone was discontinued after cardiologists’ consent. The evolution was marked by a stabilization of the visual acuity and the visual field; the papilledema completely regressed with no relapse after a two-year follow-up.
Discussion It is important to underline that patients requiring amiodarone therapy have the same vascular risk factors as those with nonarteritic anterior ischemic optic neuropathy (NAION). Symptoms of amiodarone-associated optic neuropathy share features of non-arteritic anterior ischemic optic neuropathy, the most common etiology of visual loss
with optic disk edema after the age of 50. The diagnosis of amiodarone-induced optic neuropathy should be a diagnosis of exclusion. However, some differences orient toward amiodarone-associated optic neuropathy [1—4]. As in our two cases, it occurs more often in men, while NAION has equal sex predilection. Its onset is insidious, whereas NAION is acute. Two thirds of amiodarone-associated optic neuropathy cases present bilateral optic disk edema, whereas NAION is usually unilateral. Amiodarone-induced optic neuropathy has a longer duration of disc edema, for weeks to months, as shown in our two cases. A recent review [1] has shown that the most common presentation is insidious onset, which on funduscopy generally revealed bilateral optic disk edema, although most patients reported vision loss in only one eye. In fact, ocular symptoms are varied: one third of patients were asymptomatic, some reported either acute (19%) or insidious (26%) monocular vision loss, or acute (10%) or insidious (14%) bilateral visual loss. This critical review shows that amiodarone ocular toxicity generally occurs within 1 year of drug initiation, with a median duration of 6 months before vision loss. The mechanism of amiodarone-associated optic neuropathy could be similar to amiodarone-induced peripheral neuropathy [1,4,5]: different histopathologic studies have demonstrated
Two cases of bilateral amiodarone-associated optic neuropathy
235
Figure 4. Retinophotographies of patient no 2 (top imaging): right papilledema and doubt on a left papilledema. Fluorescein angiogram (bottom imaging): bilateral fluorescein leakage in the optic nerve confirming bilateral papillitis.
Figure 5.
Kinetic perimetry of the patient no 2: bilateral visual field shrinkage, evocative of optic neuropathy.
multiple intracytoplasmic lamellar inclusions in axons of the optic nerve, with an irreversible or partially reversible toxicity. In this case, visual findings require several months to stabilize after the drug’s discontinuation. Following drug cessation, around 50% improve visual acuity, whereas around 20% have further decreased visual acuity [1]. Permanent blindness in at least one eye has been reported for 20% of affected individuals. The second mechanism can be the occurrence of a benign intracranial hypertension also called Pseudotumor cerebri [6—8]: amiodarone has been held responsible in such manifestations, in which case visual symptoms are more likely to resolve after treatment discontinuation. In our observations, an amiodarone-associated toxic neuropathy was suspected, but the mechanism remains unsure, as no lumbar puncture with cerebro-spinal
fluid pressure evaluation was performed. However, stabilization of visual symptoms with a good visual acuity argues for amiodarone implication. We note that amiodarone is frequently coadministered with digoxin, which can be an important contributing factor in the development of the toxic optic neuropathy. Digoxin similarly decreases vision and alters color perception, and its serum level is increased by amiodarone use.
Conclusion Amiodarone-induced optic neuropathy is rare but serious. There is a risk of severe vision loss and permanent blindness. Thus an ophthalmologic evaluation at baseline is
236 recommended, in particular for patients with pre-existing visual impairment. If visual symptoms develop, early referral to an ophthalmologist is recommended for evaluation of visual acuity and color vision, automated perimetry, dilated funduscopic examination, and OCT.
Disclosure of interest The authors declare that they have no conflict of interest concerning this article.
References [1] Passman RS, Bennett CL, Purpura JM, Kapur R, Johnson LN, Raisch DW, et al. Amiodarone-associated optic neuropathy: a critical review. Am J Med 2012;125:447—53.
B. Chassang et al. [2] Nagra PK, Foroozan R, Savino PJ, Castillo I, Sergott RC. Amiodarone-induced optic neuropathy. Br J Ophthalmol 2003;87:420—2. [3] Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter. J Neuroophthalmol 2005;25:232—6. [4] Johnson LN, Krohel GB, Thomas ER. The clinical spectrum of amiodarone-associated optic neuropathy. J Natl Med Assoc 2004;96:1477—91. [5] Sharma P, Sharma R. Toxic optic neuropathy. Indian J Ophthalmol 2011;59:137—41. [6] Duclos C, Bonnin N, Merlin E, Viorel A, Lacombe P, Dalens H, et al. Benign but not harmless intracranial hypertension: a case report. Arch Pediatr 2010;17:1677—81. [7] Ait Ali F, Grolleau-Raoux F, Arnaud B, Schmitt-Bernard CF. Amiodarone and disk edema: physiopathological debate based on a case report. J Fr Ophtalmol 2003;26:182—6. [8] Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol 1999;127:610—2.
Disponible en ligne sur
ScienceDirect www.sciencedirect.com
SFO COMMUNICATION
Two cases of bilateral amiodarone-associated optic neuropathy夽 À propos de deux cas de neuropathie bilatérale à l’amiodarone B. Chassang a, N. Bonnin a,∗,b, X. Moisset c, B. Citron d, P. Clavelou c, F. Chiambaretta a,b a
RMND-M2O Pole, Ophthalmology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France b EA 7281 R2D2, Biochemistery Laboratory, Medicine Faculty, Auvergne University, 63000 Clermont-Ferrand, France c RMND-M2O Pole, Neurology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France d Medical and Surgical Cardiology Pole, Cardiology department, Clermont-Ferrand University Hospital, 63000 Clermont-Ferrand, France Received 26 November 2013; accepted 9 December 2013 Available online 24 February 2014
KEYWORDS Amiodarone; Optic neuropathy; Iatrogenic disease; Papilledema
夽 ∗
Summary Introduction. — The widespread use of amiodarone is limited by its toxicity, notably to the optic nerve. We report two cases of bilateral optic nerve neuropathy due to amiodarone, and provide a detailed description of the disease. Observations. — The first case was a 59-year-old man complaining from insidious monocular loss of vision within ten months of initiating amiodarone. Funduscopy and optical coherence tomography showed bilateral optic disc edema. The second case was a 72-year-old man presenting with a decrease in visual acuity in his left eye for a month. Funduscopy showed a left optic nerve edema, and fluorescein angiography showed bilateral papillitis. In both cases, the clinical presentation was not suggestive of ischemic neuropathy, because of the preservation of visual acuity and the insidious onset. In addition, both cardiovascular and inflammatory work-up were normal. An amiodarone-associated neuropathy was suspected, and amiodarone was discontinued with the approval of the cardiologist, with complete regression of the papilledema and a stabilization of visual symptoms.
Oral communication presented at the 119th Congress of the French Society of Ophthalmology in May 2013. Corresponding author. E-mail address: [email protected] (N. Bonnin).
0181-5512/$ — see front matter © 2014 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.jfo.2013.12.004
232
B. Chassang et al. Discussion. — Differentiating between amiodarone-associated optic neuropathy and anterior ischemic optic neuropathy may be complicated by the cardiovascular background of such patients. The major criterion is the absence of a severe decrease in visual acuity; other criteria are the normality of cardiovascular and inflammatory work-up, and the improvement or the absence of worsening of symptoms after discontinuation of amiodarone. Conclusion. — Amiodarone-associated neuropathy remains a diagnosis of exclusion, and requires amiodarone discontinuation, which can only be done with the approval of a cardiologist, and sometimes requires replacement therapy. © 2014 Elsevier Masson SAS. All rights reserved.
MOTS CLÉS Amiodarone ; Neuropathie optique ; Iatrogénicité ; Œdème papillaire
Résumé Introduction. — L’amiodarone est l’anti-arythmique le plus répandu mais son utilisation est limitée par sa toxicité notamment au niveau du nerf optique. Nous rapportons deux cas de neuropathie bilatérale du nerf optique dus à l’amiodarone et à travers ces deux cas, nous apportons une description précise de la maladie. Observations. — Le premier cas est celui d’un homme de 59 ans se plaignant de baisse d’acuité visuelle insidieuse depuis dix mois après initiation d’un traitement par amiodarone. L’examen du fond d’œil montrait un œdème papillaire bilateral. Le second cas est celui d’un homme de 72 ans consultant pour une baisse d’acuité visuelle de l’œil gauche depuis un mois. L’examen du fond d’œil montrait un œdème papillaire gauche et l’angiographie à la fluorescéine confirmait l’existence d’une papillite bilatérale. Dans les deux cas, la présentation n’était pas évocatrice de neuropathie ischémique du fait de la presentation insidieuse et de la modeste baisse d’acuité visuelle. De plus, les bilans cardiovasculaires et inflammatoires étaient normaux. Une neuropathie iatrogène à l’amiodarone était suspectée et le traitement était stoppé après accord du cardiologue. Une régression de l’œdème papillaire était observée ainsi qu’une stabilisation des symptômes visuels. Discussion. — Différencier une neuropathie optique à l’amiodarone d’une neuropathie optique ischémique antérieure peut être complexe en raison des antécédents vasculaires de ces patients. Le principal critère est l’absence de baisse brutale de l’acuité visuelle; d’autres arguments tels que la normalité des bilans cardiovasculaires et inflammatoires, l’amélioration ou l’absence d’aggravation des symptômes après l’arrêt de l’amiodarone étayent le diagnostic. Conclusion. — La neuropathie iatrogène à l’amiodarone reste un diagnostic d’exclusion et impose l’arrêt d’amiodarone qui ne peut être fait qu’avec le consentement du cardiologue et nécessite parfois un traitement substitutif. © 2014 Elsevier Masson SAS. Tous droits réservés.
Introduction
Observations
Amiodarone has become a widely used class III antiarrhythmic drug. However, its use can be limited by serious toxicities and side effects, with almost 50% of long-term users resultantly discontinuing the drug [1]. Due to its lipophilic nature, amiodarone has strong tissue affinity, and its toxicity is ubiquitous, affecting the lungs, thyroid, skin, nervous system, liver, and eyes. There are a number of ocular adverse effects including corneal microdeposits, anterior subcapsular lens opacities, multiple chalazia, dry eye syndrome, halo vision and optic neuropathy [2]. Proper diagnosis of toxic optic neuropathy can justify drug withdrawal and hope of restored visual function. Every cardiologist must be aware of this potential adverse effect and ask their patients about visual symptoms.
Case 1 A 59-year-old man complained of non-painful insidious decreased vision, with a visual field defect in his right eye. This man had been undergoing amiodarone treatment (200 mg daily) for tachyarrhythmia for eleven months. He had a history of hypertension, dyslipidemia, cardiomyopathy and hyperuricemia. His medication included warfarin, bisoprolol, irbesartan, simvastatin, allopurinol and pantoprazol. Neurological examination was normal. The brain MRI was normal. Visual acuity was 20/25 in the right eye and 20/20 in the left eye. Funduscopy showed a bilateral optic disc swelling predominating on the left eye (Fig. 1). His pupils reacted equally with no relative afferent pupillary defect.
Two cases of bilateral amiodarone-associated optic neuropathy
Figure 1.
233
Retinophotographies of patient no 2. A and C. Right eye: lower-sectoral optic disc edema. B and D. Left eye: optic disc edema.
There was a central scotoma in the right visual field and an arciform scotoma in the left visual field (Fig. 2). Spectral domain optic coherency tomography (SD-OCT) showed a bilateral increase in optic nerve fiber thickness predominating on the left papilla (Fig. 3). SD-OCT is an optical signal acquisition and processing method that captures micrometer-resolution three-dimensional images from the retina. The peripapillary retina nerve fiber layer (RNFL) scan showed an increase in the left eye RNFL thickness that was above the 95th percentile of the normative data. The right eye RNFL thickness increase was sectoral, predominating on the lower quadrant. After discussion with the patient’s cardiologist, amiodarone was discontinued, and bisoprolol increased. After 3 months, the visual recovery was total,
in terms of both visual acuity and visual field, with no cardiac disturbances. Fundus examination had normalized. No relapse occurred after a four-year follow-up.
Case 2 A 72-year-old man, taking amiodarone (200 mg daily) for 8 months for atrial fibrillation, consulted our department for decreased vision in his left eye for 1 month. His medical history comprised a mantle cell lymphoma in remission, and arterial hypertension. His treatments were telmisartan and acenocoumarol. Visual acuity was measured at 20/20 in his right eye and 20/25 in his left eye. Slit lamp examination showed bilateral amiodarone corneal deposits, and
Figure 2. Kinetic perimetry of the patient no 1. Arciform scotoma in the left eye and central scotoma in the right eye, evocative of optic neuropathy.
234
B. Chassang et al.
Figure 3. Optical coherence tomography of patient no 1. Global increased left eye RNFL thickness (OS) and lower-sector increased right eye RNFL thickness (OD).
ocular pressure was normal. Fundus examination showed a papilledema in the left eye, and there was a doubt about the same aspect in the right eye (Fig. 4). Kinetic campimetry showed a significant bilateral narrowing with no special systematization (Fig. 5). Fluorescein angiogram showed a bilateral dye leakage in both optic nerves, confirming bilateral papillitis (Fig. 4). Cardiological and inflammatory assessment and brain imaging were performed, and were normal. An amiodarone-associated neuropathy was suspected, so amiodarone was discontinued after cardiologists’ consent. The evolution was marked by a stabilization of the visual acuity and the visual field; the papilledema completely regressed with no relapse after a two-year follow-up.
Discussion It is important to underline that patients requiring amiodarone therapy have the same vascular risk factors as those with nonarteritic anterior ischemic optic neuropathy (NAION). Symptoms of amiodarone-associated optic neuropathy share features of non-arteritic anterior ischemic optic neuropathy, the most common etiology of visual loss
with optic disk edema after the age of 50. The diagnosis of amiodarone-induced optic neuropathy should be a diagnosis of exclusion. However, some differences orient toward amiodarone-associated optic neuropathy [1—4]. As in our two cases, it occurs more often in men, while NAION has equal sex predilection. Its onset is insidious, whereas NAION is acute. Two thirds of amiodarone-associated optic neuropathy cases present bilateral optic disk edema, whereas NAION is usually unilateral. Amiodarone-induced optic neuropathy has a longer duration of disc edema, for weeks to months, as shown in our two cases. A recent review [1] has shown that the most common presentation is insidious onset, which on funduscopy generally revealed bilateral optic disk edema, although most patients reported vision loss in only one eye. In fact, ocular symptoms are varied: one third of patients were asymptomatic, some reported either acute (19%) or insidious (26%) monocular vision loss, or acute (10%) or insidious (14%) bilateral visual loss. This critical review shows that amiodarone ocular toxicity generally occurs within 1 year of drug initiation, with a median duration of 6 months before vision loss. The mechanism of amiodarone-associated optic neuropathy could be similar to amiodarone-induced peripheral neuropathy [1,4,5]: different histopathologic studies have demonstrated
Two cases of bilateral amiodarone-associated optic neuropathy
235
Figure 4. Retinophotographies of patient no 2 (top imaging): right papilledema and doubt on a left papilledema. Fluorescein angiogram (bottom imaging): bilateral fluorescein leakage in the optic nerve confirming bilateral papillitis.
Figure 5.
Kinetic perimetry of the patient no 2: bilateral visual field shrinkage, evocative of optic neuropathy.
multiple intracytoplasmic lamellar inclusions in axons of the optic nerve, with an irreversible or partially reversible toxicity. In this case, visual findings require several months to stabilize after the drug’s discontinuation. Following drug cessation, around 50% improve visual acuity, whereas around 20% have further decreased visual acuity [1]. Permanent blindness in at least one eye has been reported for 20% of affected individuals. The second mechanism can be the occurrence of a benign intracranial hypertension also called Pseudotumor cerebri [6—8]: amiodarone has been held responsible in such manifestations, in which case visual symptoms are more likely to resolve after treatment discontinuation. In our observations, an amiodarone-associated toxic neuropathy was suspected, but the mechanism remains unsure, as no lumbar puncture with cerebro-spinal
fluid pressure evaluation was performed. However, stabilization of visual symptoms with a good visual acuity argues for amiodarone implication. We note that amiodarone is frequently coadministered with digoxin, which can be an important contributing factor in the development of the toxic optic neuropathy. Digoxin similarly decreases vision and alters color perception, and its serum level is increased by amiodarone use.
Conclusion Amiodarone-induced optic neuropathy is rare but serious. There is a risk of severe vision loss and permanent blindness. Thus an ophthalmologic evaluation at baseline is
236 recommended, in particular for patients with pre-existing visual impairment. If visual symptoms develop, early referral to an ophthalmologist is recommended for evaluation of visual acuity and color vision, automated perimetry, dilated funduscopic examination, and OCT.
Disclosure of interest The authors declare that they have no conflict of interest concerning this article.
References [1] Passman RS, Bennett CL, Purpura JM, Kapur R, Johnson LN, Raisch DW, et al. Amiodarone-associated optic neuropathy: a critical review. Am J Med 2012;125:447—53.
B. Chassang et al. [2] Nagra PK, Foroozan R, Savino PJ, Castillo I, Sergott RC. Amiodarone-induced optic neuropathy. Br J Ophthalmol 2003;87:420—2. [3] Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter. J Neuroophthalmol 2005;25:232—6. [4] Johnson LN, Krohel GB, Thomas ER. The clinical spectrum of amiodarone-associated optic neuropathy. J Natl Med Assoc 2004;96:1477—91. [5] Sharma P, Sharma R. Toxic optic neuropathy. Indian J Ophthalmol 2011;59:137—41. [6] Duclos C, Bonnin N, Merlin E, Viorel A, Lacombe P, Dalens H, et al. Benign but not harmless intracranial hypertension: a case report. Arch Pediatr 2010;17:1677—81. [7] Ait Ali F, Grolleau-Raoux F, Arnaud B, Schmitt-Bernard CF. Amiodarone and disk edema: physiopathological debate based on a case report. J Fr Ophtalmol 2003;26:182—6. [8] Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol 1999;127:610—2.
