- Email: [email protected]
Enhancement of the optic nerve sheath and temporal arteries from giant cell arteritis
Correspondence 5. Materin MA, Shields CL, Marr BP, Demirci H, Shields JA. Retinal racemose hemangioma. Retina. 2005;25:936-7. 6. Telander DG, Choi SS, Zawadzki RJ, Berger N, Keltner JL, Werner JS. Microstructural abnormalities revealed by high resolution imaging systems in central macular arteriovenous malformation. Ophthalmic Surg Lasers Imaging. 2010;9:1-4. 7. Qin XJ, Huang C, Lai K. Retinal vein occlusion in retinal racemose hemangioma: a case report and literature review of ocular complications in this rare retinal vascular disorder. BMC Ophthalmol. 2014;14:101. 8. Mansour AM, Wells CG, Jampol LM, Kalina RE. Ocular complications of arteriovenous communications of the retina. Arch Ophthalmol. 1989;107:232-6.
Enhancement of the optic nerve sheath and temporal arteries from giant cell arteritis We report a patient who developed sequential severe painless vision loss from giant cell arteritis (GCA) who had optic nerve sheath enhancement on magnetic resonance imaging (MRI), which has only rarely been reported in the past. In addition, the MRI showed fusiform enlargement of the temporal arteries bilaterally that can be used to confirm the diagnosis of GCA.
9. Schatz H, Chang LF, Ober RR, McDonald HR, Johnson RN. Central retinal vein occlusion associated with retinal arteriovenous malformation. Ophthalmology. 1993;100:24-30. 10. Sarraf D, Rahimy E, Fawzi AA, et al. Paracentral acute middle maculopathy: a new variant of acute macular neuroretinopathy associated with retinal capillary ischemia. JAMA Ophthalmol. 2013;131:1275-87. Can J Ophthalmol 2015;50:e93–e96 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2015.06.008
A 79-year-old female was referred for sequential severe painless vision loss in both eyes. She had no significant medical history or medications. A week before initial presentation, she noted decreased vision in the right eye. Two days later, she developed vision loss in the left eye. She was seen by her local ophthalmologist and found to have bilateral disc edema with visual acuity of hand motion OD and 20/40 OS with a large relative afferent pupillary defect OD. MRI demonstrated enhancement of the optic nerve sheaths bilaterally (Fig. 1). The Erythrocyte sedimentation
Fig. 1 — Magnetic resonance imaging T1-weighted with contrast shows bilateral optic nerve sheath enlargement and enhancement on both axial (A) and coronal images (B) (red arrows). The axial images also show bilateral fusiform enlargement and enhancement of the temporal arteries (white arrows). Fundus photography demonstrates bilateral pallid disc edema (C, D) with a few peripapillary hemorrhages in the right eye (C).
e96
CAN J OPHTHALMOL — VOL. 50, NO. 5, OCTOBER 2015
Correspondence rate (ESR) was 106 and C-reactive protein (CRP) was 90 mg/L. She denied headaches, scalp tenderness, jaw claudication, fevers, unexplained weight loss, and proximal muscle weakness. Despite a lack of systemic symptoms of GCA, she was started on 60 mg prednisone with a suspicion for either GCA or inflammatory optic neuropathy. Because of the optic nerve sheath enhancement on MRI, she also underwent a lumbar puncture and blood work-up for infectious and inflammatory causes; results were unremarkable. She continued to have worsening vision over 3 days despite the oral prednisone and was therefore given 1 g intravenous methylprednisolone. She was evaluated in neuro-ophthalmology clinic the following day, and visual acuity had worsened to light perception OU. The pupils responded minimally to light, and there was no relative afferent pupillary defect. Dilated eye examination showed pallid disc edema OU (Fig. 1). The patient underwent temporal artery biopsy that showed active granulomatous inflammation and transmural scarring, which confirmed the diagnosis of bilateral arteritic anterior ischemic optic neuropathy from GCA. After further review of the MRI scan, fusiform enlargement of the temporal arteries was noted, which could have led to an earlier definitive diagnosis of GCA (Fig. 1). Our case demonstrates a case of bilateral arteritic anterior ischemic optic neuropathy from GCA despite a lack of systemic symptoms. In addition, there was optic nerve sheath enhancement and fusiform enlargement of the temporal arteries bilaterally on MRI. Although we do not advocate routine MRI on patients with classic GCA, if the imaging has already been performed or if there is diagnostic uncertainty, enlargement or enhancement of the temporal arteries can help confirm the diagnosis of GCA. Recent studies have demonstrated that mural enhancement of the temporal arteries on MRI has a sensitivity of 80.6% and specificity of 97% for GCA.1,2 Theoretically, the imaging findings could even guide the location of temporal artery biopsies.1 It is also important to note that optic nerve sheath enhancement and enlargement can be seen in GCA. Optic
nerve sheath enhancement has been previously reported in 3 case reports, initially described by Lee in 1999.3–5 The optic nerve sheath enhancement likely results from the same process of granulomatous inflammation that is seen in the temporal arteries, which leads to disruption of the blood–optic nerve barrier. This finding on MRI could incorrectly lead the ophthalmologist who is unaware of possible optic nerve sheath enhancement and enlargement from GCA to suspect an inflammatory condition such as sarcoidosis or Wegener granulomatosis. Looking for coinciding fusiform enlargement of the temporal arteries can alleviate any diagnostic uncertainty.
External ocular infections due to methicillinresistant Staphylococcus aureus and medical history
determine the susceptibility of the isolates; to administer effective agents as the initial treatment, it is desirable to detect a possible MRSA infection by analyzing clinical information. It has been reported that the risk factors for MRSA ocular infection are a history of health care exposure7 and the following 3 conditions: an ocular surface disease, malignancy, and a debilitating medical illness.8 This study aimed to determine the MRSA culture-positive rate among patients with suspected external ocular infections and to investigate whether a history of MRSA infection is a predictor of external ocular MRSA infection.
Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most important human bacterial pathogens due to its multiple drug resistance, perceived increasing prevalence, and high mortality rate.1,2 As a pathogen in external ocular infections such as keratitis, conjunctivitis, and those involving lid and lacrimal system disorders, MRSA is an increasingly prevalent type of S. aureus infection.3–6 It takes several days to identify the causative bacteria and to
John J. Chen, *,† Randy H. Kardon, *,‡ Timothy J. Daley, § Reid A. Longmuir * *
University of Iowa, Iowa City, Iowa; †Mayo Clinic; Department of Veterans Affairs, Rochester, Minnesota, Iowa City; ‡Department of Veterans Affairs, Iowa City; §Medical Associates, Dubuque, Iowa Correspondence to: Reid A. Longmuir, MD: [email protected]
REFERENCES 1. Bley TA, Uhl M, Carew J, et al. Diagnostic value of high-resolution MR imaging in giant cell arteritis. AJNR Am J Neuroradiol. 2007;28:1722-7. 2. Al-Zubidi N, Mai C, Haykal HA, Lee AG. Temporal artery enhancement on cranial magnetic resonance imaging. Can J Ophthalmol. 2014;49:e63-5. 3. Morgenstern KE, Ellis BD, Schochet SS, Linberg JV. Bilateral optic nerve sheath enhancement from giant cell arteritis. J Rheumatol. 2003;30:625-7. 4. Liu KC, Chesnutt DA. Perineural optic nerve enhancement on magnetic resonance imaging in giant cell arteritis. J Neuroophthalmol. 2013;33:279-81. 5. Lee AG, Eggenberger ER, Kaufman DI, Manrique C. Optic nerve enhancement on magnetic resonance imaging in arteritic ischemic optic neuropathy. J Neuro-ophthalmol. 1999;19:235-7. Can J Ophthalmol 2015;50:e96–e97 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2015.07.007
CAN J OPHTHALMOL — VOL. 50, NO. 5, OCTOBER 2015
e97
Enhancement of the optic nerve sheath and temporal arteries from giant cell arteritis We report a patient who developed sequential severe painless vision loss from giant cell arteritis (GCA) who had optic nerve sheath enhancement on magnetic resonance imaging (MRI), which has only rarely been reported in the past. In addition, the MRI showed fusiform enlargement of the temporal arteries bilaterally that can be used to confirm the diagnosis of GCA.
9. Schatz H, Chang LF, Ober RR, McDonald HR, Johnson RN. Central retinal vein occlusion associated with retinal arteriovenous malformation. Ophthalmology. 1993;100:24-30. 10. Sarraf D, Rahimy E, Fawzi AA, et al. Paracentral acute middle maculopathy: a new variant of acute macular neuroretinopathy associated with retinal capillary ischemia. JAMA Ophthalmol. 2013;131:1275-87. Can J Ophthalmol 2015;50:e93–e96 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2015.06.008
A 79-year-old female was referred for sequential severe painless vision loss in both eyes. She had no significant medical history or medications. A week before initial presentation, she noted decreased vision in the right eye. Two days later, she developed vision loss in the left eye. She was seen by her local ophthalmologist and found to have bilateral disc edema with visual acuity of hand motion OD and 20/40 OS with a large relative afferent pupillary defect OD. MRI demonstrated enhancement of the optic nerve sheaths bilaterally (Fig. 1). The Erythrocyte sedimentation
Fig. 1 — Magnetic resonance imaging T1-weighted with contrast shows bilateral optic nerve sheath enlargement and enhancement on both axial (A) and coronal images (B) (red arrows). The axial images also show bilateral fusiform enlargement and enhancement of the temporal arteries (white arrows). Fundus photography demonstrates bilateral pallid disc edema (C, D) with a few peripapillary hemorrhages in the right eye (C).
e96
CAN J OPHTHALMOL — VOL. 50, NO. 5, OCTOBER 2015
Correspondence rate (ESR) was 106 and C-reactive protein (CRP) was 90 mg/L. She denied headaches, scalp tenderness, jaw claudication, fevers, unexplained weight loss, and proximal muscle weakness. Despite a lack of systemic symptoms of GCA, she was started on 60 mg prednisone with a suspicion for either GCA or inflammatory optic neuropathy. Because of the optic nerve sheath enhancement on MRI, she also underwent a lumbar puncture and blood work-up for infectious and inflammatory causes; results were unremarkable. She continued to have worsening vision over 3 days despite the oral prednisone and was therefore given 1 g intravenous methylprednisolone. She was evaluated in neuro-ophthalmology clinic the following day, and visual acuity had worsened to light perception OU. The pupils responded minimally to light, and there was no relative afferent pupillary defect. Dilated eye examination showed pallid disc edema OU (Fig. 1). The patient underwent temporal artery biopsy that showed active granulomatous inflammation and transmural scarring, which confirmed the diagnosis of bilateral arteritic anterior ischemic optic neuropathy from GCA. After further review of the MRI scan, fusiform enlargement of the temporal arteries was noted, which could have led to an earlier definitive diagnosis of GCA (Fig. 1). Our case demonstrates a case of bilateral arteritic anterior ischemic optic neuropathy from GCA despite a lack of systemic symptoms. In addition, there was optic nerve sheath enhancement and fusiform enlargement of the temporal arteries bilaterally on MRI. Although we do not advocate routine MRI on patients with classic GCA, if the imaging has already been performed or if there is diagnostic uncertainty, enlargement or enhancement of the temporal arteries can help confirm the diagnosis of GCA. Recent studies have demonstrated that mural enhancement of the temporal arteries on MRI has a sensitivity of 80.6% and specificity of 97% for GCA.1,2 Theoretically, the imaging findings could even guide the location of temporal artery biopsies.1 It is also important to note that optic nerve sheath enhancement and enlargement can be seen in GCA. Optic
nerve sheath enhancement has been previously reported in 3 case reports, initially described by Lee in 1999.3–5 The optic nerve sheath enhancement likely results from the same process of granulomatous inflammation that is seen in the temporal arteries, which leads to disruption of the blood–optic nerve barrier. This finding on MRI could incorrectly lead the ophthalmologist who is unaware of possible optic nerve sheath enhancement and enlargement from GCA to suspect an inflammatory condition such as sarcoidosis or Wegener granulomatosis. Looking for coinciding fusiform enlargement of the temporal arteries can alleviate any diagnostic uncertainty.
External ocular infections due to methicillinresistant Staphylococcus aureus and medical history
determine the susceptibility of the isolates; to administer effective agents as the initial treatment, it is desirable to detect a possible MRSA infection by analyzing clinical information. It has been reported that the risk factors for MRSA ocular infection are a history of health care exposure7 and the following 3 conditions: an ocular surface disease, malignancy, and a debilitating medical illness.8 This study aimed to determine the MRSA culture-positive rate among patients with suspected external ocular infections and to investigate whether a history of MRSA infection is a predictor of external ocular MRSA infection.
Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most important human bacterial pathogens due to its multiple drug resistance, perceived increasing prevalence, and high mortality rate.1,2 As a pathogen in external ocular infections such as keratitis, conjunctivitis, and those involving lid and lacrimal system disorders, MRSA is an increasingly prevalent type of S. aureus infection.3–6 It takes several days to identify the causative bacteria and to
John J. Chen, *,† Randy H. Kardon, *,‡ Timothy J. Daley, § Reid A. Longmuir * *
University of Iowa, Iowa City, Iowa; †Mayo Clinic; Department of Veterans Affairs, Rochester, Minnesota, Iowa City; ‡Department of Veterans Affairs, Iowa City; §Medical Associates, Dubuque, Iowa Correspondence to: Reid A. Longmuir, MD: [email protected]
REFERENCES 1. Bley TA, Uhl M, Carew J, et al. Diagnostic value of high-resolution MR imaging in giant cell arteritis. AJNR Am J Neuroradiol. 2007;28:1722-7. 2. Al-Zubidi N, Mai C, Haykal HA, Lee AG. Temporal artery enhancement on cranial magnetic resonance imaging. Can J Ophthalmol. 2014;49:e63-5. 3. Morgenstern KE, Ellis BD, Schochet SS, Linberg JV. Bilateral optic nerve sheath enhancement from giant cell arteritis. J Rheumatol. 2003;30:625-7. 4. Liu KC, Chesnutt DA. Perineural optic nerve enhancement on magnetic resonance imaging in giant cell arteritis. J Neuroophthalmol. 2013;33:279-81. 5. Lee AG, Eggenberger ER, Kaufman DI, Manrique C. Optic nerve enhancement on magnetic resonance imaging in arteritic ischemic optic neuropathy. J Neuro-ophthalmol. 1999;19:235-7. Can J Ophthalmol 2015;50:e96–e97 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2015.07.007
CAN J OPHTHALMOL — VOL. 50, NO. 5, OCTOBER 2015
e97