SUDDEN VISUAL LOSS AFTER INTRAVITREAL TRIAMCINOLONE Thushanthi Ramakrishnan, MBBS,* Kira Michalova, MD, FRANZCO,* Anthony J.H. Hall, MD, FRANZCO*†
Purpose: To report a case of sudden loss of vision after intravitreal triamcinolone for the management of cystoid macular edema secondary to a central retinal vein occlusion with subsequent development of nonarteritic anterior ischemic optic neuropathy. Method: Retrospective case report. Conclusion: The pathophysiology of nonarteritic anterior ischemic optic neuropathy (NAION) still remains controversial. Our report does not allow any conclusion about a direct causal relationship, however we postulate a contributory role of intrvitreal triamcinolone in the development of NAION in our patient. RETINAL CASES & BRIEF REPORTS 6:85–86, 2012
Worth, TX). Two days after the injection, she noticed a transient improvement in her vision (not documented), but on the third day, she noted sudden loss of vision of her left eye. Her medical history included atrial fibrillation for which she was anticoagulated, cerebral small vessel ischemia, and hypothyroidism. On examination, her visual acuity in the left eye was perception of light only. A left relative afferent pupillary defect was present, and intraocular pressure in the left eye was 16 mmHg. Fundus examination of this eye showed persisting signs of central retinal vein occlusion with disk edema and retinal hemorrhages in four quadrants and a decrease in macular edema (Figure 1, A and B). Laboratory testing showed erythrocyte sedimentation rate of 70, C-reactive protein of 8, and platelet count of 155. Although no clinical signs or symptoms of giant cell arteritis were present, a temporal artery biopsy was recommended but declined by the patient. On review 3 months later, she had a left visual acuity of count fingers at 1/3 meter, and fundoscopy showed a pale disk with no disk cupping. She had no symptoms of giant cell arteritis, and her inflammatory markers were normal. A presumed diagnosis of left NAION was made.
From the *Department of Ophthalmology, Alfred Hospital, Melbourne, Australia; and †Department of Surgery, Monash University, Melbourne, Australia.
T
riamcinolone acetonide has been used intravitreally to treat a wide range of posterior segment diseases. Recently, the SCORE study1 showed its beneficial effect in the treatment of cystoid macular edema secondary to a central retinal vein occlusion (CRVO). We present a case of profound visual loss after intravitreal triamcinolone (IVTA) injection for this indication, in a patient with characteristics similar to those of the SCORE cohort. Case Report An 82-year-old woman presented with sudden loss of vision in her left eye 3 days after being treated with IVTA for the management of cystoid macular edema secondary to CRVO. Her ocular history included nonarteritic anterior ischemic optic neuropathy (NAION) of the right eye 3 years ago with residual right visual acuity of hand movements. Temporal artery biopsy at that time was negative for giant cell arteritis. She had uneventful left cataract surgery 6 months before the current presentation, resulting in a corrected visual acuity of 20/15. A month later, she developed a left CRVO with a visual acuity of 20/60. The left CRVO was observed for 2 months without treatment, but the vision continued to deteriorate (20/80) as she developed cystoid macular edema (central macular thickness of 571 mm on OCT). She was then treated with 4 mg/0.1 mL of IVTA (Triesence, Alcon, Fort
Discussion NAION is the most common acute optic neuropathy in adults older than 50 years with an annual incidence of 10 per 100,000.2 However, many aspects of the disease remain poorly understood including the pathophysiology. NAION is believed to occur as a result of infarction of the retrolaminar portion of the optic nerve head. The final pathway is a compartment syndrome with axonal edema leading to axonal degeneration and apoptosis of the retinal ganglion cells.3 While the mechanisms that lead to this final pathway remain contentious, recently, it has been hypothesized that NAION is primarily a venous occlusive disease, caused by a closure of tributary
None of the authors have any conflict of interest. Reprint requests: Thushanthi Ramakrishnan, MBBS, Alfred Hospital, Commercial RoadPrahran VIC 3181, Australia; e-mail: [email protected]
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Fig. 1. A. Color fundus photograph. B. Fluorescein angiography of the left eye before IVTA treatment showing signs of CRVO with macular edema. C. Color fundus photograph. D. Fluorescein angiography of the left eye 1 week after IVTA injection showing decrease in macular edema with persistent signs of CRVO.
venules that drain into the central retinal vein posterior to the surface of the optic nerve head.4 Predisposing risk factors for NAION include a small cup-to-disk ratio (#0.2), diabetes, obstructive sleep apnea, prolonged surgical procedures, and certain medications.3 The ischemic optic neuropathy decompression trial follow-up study evaluated the risk factors for development of NAION in the second eye.5 The study reported the risk of sequential NAION in the fellow eye to be 15% in 5 years. The predisposing factors were independent of the primary risk factors and included diabetes and poor visual acuity in the first eye (20/200 or worse). Our patient had an underlying ‘‘disk at risk’’ and was at increased risk of developing NAION in the left eye as she had a poor visual outcome in her first affected eye. Furthermore, the CRVO may have also contributed to the ischemic optic neuropathy by potentially compromising the prepapillary capillaries. Also of note is that although the patient was asymptomatic, given an elevated erythrocyte sedimentation rate of 70, a diagnosis of giant cell arteritis cannot be completely excluded. The question remains as to what role the IVTA played in the pathogenesis of the ischemic event in the second eye. To the best of our knowledge, no case of NAION after therapy with IVTA has been reported in literature. The pathophysiologic assessment of NAION still remains controversial, and our report does not allow any conclusion about a direct causal relationship between
IVTA and NAION. It can be argued that in this patient, the correlation between the two entities may have been purely coincidental. However, given the temporal association between the treatment with IVTA and the onset of the symptoms, a high index of suspicion is raised toward a contributory role of the IVTA in the development of NAION. In the setting of a ‘‘disk at risk’’ with swelling from the CRVO, we hypothesize that a transient rise in intraocular pressure at the time of injection may have been the final catalyst in the development of NAION. Key words: intravitreal triamcinolone, loss of vision, NAION. References 1. Scott IU, Ip MS, VanVeldhuisen PC, et al. A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with standard care to treat vision loss associated with macular edema secondary to central retinal vein occlusion. Arch Ophthalmol 2009;127:1115–1128. 2. Hattenhauer MG, Leavitt JA, Hodge DO, Grill R, Gray DT. Incidence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123:103–107. 3. Kerr NM, Chew SSSL, Danesh-Meyer HV. Non-arteritic anterior ischaemic optic neuropathy: a review and update. J Clin Neurosci 2009;16:994–1000. 4. Levin LA, Danesh-Meyer HV. Hypothesis: a venous origin for non-arteritic ischaemic optic neuropathy. Arch Ophthalmol 2008;126:1582–1585. 5. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up study. Am J Ophthalmol 2002;134:317–328.
Purpose: To report a case of sudden loss of vision after intravitreal triamcinolone for the management of cystoid macular edema secondary to a central retinal vein occlusion with subsequent development of nonarteritic anterior ischemic optic neuropathy. Method: Retrospective case report. Conclusion: The pathophysiology of nonarteritic anterior ischemic optic neuropathy (NAION) still remains controversial. Our report does not allow any conclusion about a direct causal relationship, however we postulate a contributory role of intrvitreal triamcinolone in the development of NAION in our patient. RETINAL CASES & BRIEF REPORTS 6:85–86, 2012
Worth, TX). Two days after the injection, she noticed a transient improvement in her vision (not documented), but on the third day, she noted sudden loss of vision of her left eye. Her medical history included atrial fibrillation for which she was anticoagulated, cerebral small vessel ischemia, and hypothyroidism. On examination, her visual acuity in the left eye was perception of light only. A left relative afferent pupillary defect was present, and intraocular pressure in the left eye was 16 mmHg. Fundus examination of this eye showed persisting signs of central retinal vein occlusion with disk edema and retinal hemorrhages in four quadrants and a decrease in macular edema (Figure 1, A and B). Laboratory testing showed erythrocyte sedimentation rate of 70, C-reactive protein of 8, and platelet count of 155. Although no clinical signs or symptoms of giant cell arteritis were present, a temporal artery biopsy was recommended but declined by the patient. On review 3 months later, she had a left visual acuity of count fingers at 1/3 meter, and fundoscopy showed a pale disk with no disk cupping. She had no symptoms of giant cell arteritis, and her inflammatory markers were normal. A presumed diagnosis of left NAION was made.
From the *Department of Ophthalmology, Alfred Hospital, Melbourne, Australia; and †Department of Surgery, Monash University, Melbourne, Australia.
T
riamcinolone acetonide has been used intravitreally to treat a wide range of posterior segment diseases. Recently, the SCORE study1 showed its beneficial effect in the treatment of cystoid macular edema secondary to a central retinal vein occlusion (CRVO). We present a case of profound visual loss after intravitreal triamcinolone (IVTA) injection for this indication, in a patient with characteristics similar to those of the SCORE cohort. Case Report An 82-year-old woman presented with sudden loss of vision in her left eye 3 days after being treated with IVTA for the management of cystoid macular edema secondary to CRVO. Her ocular history included nonarteritic anterior ischemic optic neuropathy (NAION) of the right eye 3 years ago with residual right visual acuity of hand movements. Temporal artery biopsy at that time was negative for giant cell arteritis. She had uneventful left cataract surgery 6 months before the current presentation, resulting in a corrected visual acuity of 20/15. A month later, she developed a left CRVO with a visual acuity of 20/60. The left CRVO was observed for 2 months without treatment, but the vision continued to deteriorate (20/80) as she developed cystoid macular edema (central macular thickness of 571 mm on OCT). She was then treated with 4 mg/0.1 mL of IVTA (Triesence, Alcon, Fort
Discussion NAION is the most common acute optic neuropathy in adults older than 50 years with an annual incidence of 10 per 100,000.2 However, many aspects of the disease remain poorly understood including the pathophysiology. NAION is believed to occur as a result of infarction of the retrolaminar portion of the optic nerve head. The final pathway is a compartment syndrome with axonal edema leading to axonal degeneration and apoptosis of the retinal ganglion cells.3 While the mechanisms that lead to this final pathway remain contentious, recently, it has been hypothesized that NAION is primarily a venous occlusive disease, caused by a closure of tributary
None of the authors have any conflict of interest. Reprint requests: Thushanthi Ramakrishnan, MBBS, Alfred Hospital, Commercial RoadPrahran VIC 3181, Australia; e-mail: [email protected]
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Fig. 1. A. Color fundus photograph. B. Fluorescein angiography of the left eye before IVTA treatment showing signs of CRVO with macular edema. C. Color fundus photograph. D. Fluorescein angiography of the left eye 1 week after IVTA injection showing decrease in macular edema with persistent signs of CRVO.
venules that drain into the central retinal vein posterior to the surface of the optic nerve head.4 Predisposing risk factors for NAION include a small cup-to-disk ratio (#0.2), diabetes, obstructive sleep apnea, prolonged surgical procedures, and certain medications.3 The ischemic optic neuropathy decompression trial follow-up study evaluated the risk factors for development of NAION in the second eye.5 The study reported the risk of sequential NAION in the fellow eye to be 15% in 5 years. The predisposing factors were independent of the primary risk factors and included diabetes and poor visual acuity in the first eye (20/200 or worse). Our patient had an underlying ‘‘disk at risk’’ and was at increased risk of developing NAION in the left eye as she had a poor visual outcome in her first affected eye. Furthermore, the CRVO may have also contributed to the ischemic optic neuropathy by potentially compromising the prepapillary capillaries. Also of note is that although the patient was asymptomatic, given an elevated erythrocyte sedimentation rate of 70, a diagnosis of giant cell arteritis cannot be completely excluded. The question remains as to what role the IVTA played in the pathogenesis of the ischemic event in the second eye. To the best of our knowledge, no case of NAION after therapy with IVTA has been reported in literature. The pathophysiologic assessment of NAION still remains controversial, and our report does not allow any conclusion about a direct causal relationship between
IVTA and NAION. It can be argued that in this patient, the correlation between the two entities may have been purely coincidental. However, given the temporal association between the treatment with IVTA and the onset of the symptoms, a high index of suspicion is raised toward a contributory role of the IVTA in the development of NAION. In the setting of a ‘‘disk at risk’’ with swelling from the CRVO, we hypothesize that a transient rise in intraocular pressure at the time of injection may have been the final catalyst in the development of NAION. Key words: intravitreal triamcinolone, loss of vision, NAION. References 1. Scott IU, Ip MS, VanVeldhuisen PC, et al. A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with standard care to treat vision loss associated with macular edema secondary to central retinal vein occlusion. Arch Ophthalmol 2009;127:1115–1128. 2. Hattenhauer MG, Leavitt JA, Hodge DO, Grill R, Gray DT. Incidence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123:103–107. 3. Kerr NM, Chew SSSL, Danesh-Meyer HV. Non-arteritic anterior ischaemic optic neuropathy: a review and update. J Clin Neurosci 2009;16:994–1000. 4. Levin LA, Danesh-Meyer HV. Hypothesis: a venous origin for non-arteritic ischaemic optic neuropathy. Arch Ophthalmol 2008;126:1582–1585. 5. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up study. Am J Ophthalmol 2002;134:317–328.
