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Year : 2021  |  Volume : 1  |  Issue : 4  |  Page : 771-773

Anterior ischemic optic neuropathy secondary to optic nerve head drusen - A case report and review of literature

Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh, India

Date of Submission06-Jan-2021
Date of Acceptance10-Jun-2021
Date of Web Publication09-Oct-2021

Correspondence Address:
Dr. Sanjiv Kumar Gupta
Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_3795_20

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Herein, we report a case of acute, unilateral, painless visual loss in a middle-aged female. A 43-year-old female presented with rapid painless diminution of vision in the left eye with no history of any systemic disease. Anterior segment findings were within the normal limit in both eyes. Fundus examination revealed hemorrhages at the disc with pale disc and disc edema in the left eye and no remarkable change in the right eye. Ultrasound B-scan (USG) and computed tomography (CT) scan revealed optic nerve head drusen (ONHD). Diagnosis of nonarteritic anterior ischemic optic neuropathy (NAION) secondary to ONHD of the left eye was made.

Keywords: Nonarteritic anterior ischemic optic neuropathy, optic nerve head drusen, painless visual loss

How to cite this article:
Gupta D, Chaubey A, Singh R, Gupta SK. Anterior ischemic optic neuropathy secondary to optic nerve head drusen - A case report and review of literature. Indian J Ophthalmol Case Rep 2021;1:771-3

How to cite this URL:
Gupta D, Chaubey A, Singh R, Gupta SK. Anterior ischemic optic neuropathy secondary to optic nerve head drusen - A case report and review of literature. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Oct 19];1:771-3. Available from: https://www.ijoreports.in/text.asp?2021/1/4/771/327638

Optic nerve head drusen (ONHD) are globular, laminated, often calcified hyaline bodies and can be of two types: superficial and deep.[1] The overall prevalence of ONHD in the general population is 1.8%–2.0%, but in only 0.2%–0.3% population, they can be visualized by fundus examination.[2] The probability of finding ONHD in a crowded optic disc with a significantly smaller cup disc ratio is high.[3] Clinical suspicion aided with diagnostic tools like USG, fundus autofluorescence, and CT scan orbit can help in establishing the diagnosis.[4] Recently, enhanced depth imaging optical coherence tomography of the optic nerve head has emerged as a more sensitive and accurate diagnostic tool for ONHD.[5] Generally, ONHD does not cause any significant visual symptoms and is coincidentally found with visual field defects in 87% of affected eyes.[6] But rarely, it can present as sudden painless visual loss, manifesting as ONHD with NAION.[7]

  Case Report Top

A 43-year-old female patient reported to the outpatient department with complaints of rapid diminution of vision in the left eye (LE) for the last few days, which was noticed on waking up in the morning. There were no other ocular complaints or systemic diseases.

After obtaining proper written informed consent, the patient was examined. On examination, the anterior segment was within normal limits in both eyes except for a relative afferent pupillary defect in the LE. Visual acuity was finger count close to face and near acuity <N 36 in the LE with no improvement and 20/60 and N-8 in the right eye (RE), improving to 20/20 with + 0.75 DS with + 1 DS near add in RE. Fundus examination revealed hemorrhages at the disc with pale disc and disc edema in the LE, no significant findings in the periphery, and no remarkable changes seen in the fundus of RE [Figure 1]. A provisional diagnosis of NAION in the LE was considered as there was no scalp tenderness and no symptoms suggestive of jaw claudication.

Complete hemogram, CT scan skull and orbit, USG, visual field examination by automated static perimetry, and fluorescein fundus angiography (FFA) were obtained. The hemogram (including coagulation profile) was normal except for mild anemia with hemoglobin of 10.2 gm%, the erythrocyte sedimentation rate (ESR) was 22 mm, and c-reactive protein was 1 mg/L which was within normal limits.
Figure 1: Fundus photograph showing normal fundus of the right eye and disc pallor with 360° blurred margins (black arrow) and inferior disc hemorrhages (blue arrow) of the left eye

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On FFA, arm to retina time was 12 s. The late phase showed staining of the optic disc as evidence of disc edema in the LE. The RE angiography was unremarkable. The USG of the LE revealed a highly reflective small echogenic shadow at the commencement of the optic nerve, which measured 1.3 mm axially. Echogenicity persisted even at low gains [Figure 2]. Similar findings were seen on CT scan orbit as a radiolucent shadow at the optic nerve head in the LE [Figure 3]. The visual field examination could not be performed in the LE due to poor vision. The findings were suggestive of ONHD in the LE with NAION. The patient was put on oral prednisolone 1 mg/kg body weight with 1500 m sublingual methylcobalamine. Retrobulbar injection of dexamethasone 2 mg was instituted, 5 doses every alternate day. The vision in the LE improved on treatment to 6/12 during a period of 2 weeks. The steroids were tapered and stopped when there was no further symptomatic improvement during 1 week.
Figure 2: B-Scan ultrasonography of the left eye revealing highly reflective small echogenic shadow at the commencement of optic nerve (red arrow)

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Figure 3: Axial noncontrast CT scan of orbit depicting small hyperdense lesion at left optic nerve head (red arrow)

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At follow-up after 1 month, the patient's vision was unchanged and maintained at 6/12. Visual field examination by automated static perimetry revealed a superior absolute field defect with macular sparing [Figure 4]. The field examination findings correlated with the sectoral involvement of the optic disc at the first visit [Figure 1]. The disc edema had subsided and the hemorrhages at disc had disappeared. Till reporting, patient was still on tab methylcobalamine 1500 m once daily for the last 2 months.
Figure 4: Static automated perimetry of the left eye demonstrating a superior absolute field defect with macular sparing

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  Discussion Top

ONHD manifests as insidious vision loss, usually characterized by subclinical visual field defect associated with peripapillary Retinal nerve fiber layer (RNFL) loss.[8] In most of these cases, it may resemble glaucomatous field loss.[7] Whereas, sudden and severe visual loss, although unusual, can occur in association with complications such as NAION, retinal hemorrhages, and subretinal neovascular membrane.[9]

ONHD represents a disc anomaly in which the head is crowded and cupless. A study by Purvin et al.[7] showed that the mean age of NAION associated with drusen was 49.4 years, in contrast with previous studies done in patients of NAION without drusen, in whom the mean age was 63.4 years. Purvin et al.[7] concluded that patients of NAION associated with ONHD were younger, have more favorable prognosis, and were more likely to be associated with preceding episodes of transient visual obscuration. Some of these characteristics are present in our case such as the patient presented with visual loss at the age of 43 years, which was earlier than the normal presentation of NAION and favorable prognosis as patient's vision improved to 6/12 from finger count after steroid treatment. In our case, ONHD was deeply buried and the diagnosis was established on the basis of USG and CT scan. Besides NAION, optic neuritis can also be a differential diagnosis, which may require further extensive neurological work.

  Conclusion Top

In conclusion, our case shows that deeply buried ONHD can play an important role in the etiology of sudden visual loss and optic disc edema in young individuals where clinical diagnosis is difficult on routine examination. Hence, we should be vigilant of this mimicker of optic neuritis and papilledema, to avoid unnecessary neurological testing and minimize the risk of mismanagement.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Sato T, Mrejen S, Spaide RF. Multimodal imaging of optic disc drusen. Am J Ophthalmol 2013;156:275-82.e1.  Back to cited text no. 1
Auw-Haedrich C, Staubach F, Witschel H. Optic disk drusen. Surv Ophthalmol 2002;47:515–532.  Back to cited text no. 2
Wilkins JM, Pomeranz HD. Visual manifestations of visible and buried optic disc drusen. J Neuroophthalmol 2004;24:125-9.  Back to cited text no. 3
Loft FC, Malmqvist L, Wessel Lindberg AS, Hamann S. The influence of volume and anatomic location of optic disc drusen on the sensitivity of autofluorescence. J Neuroophthalmol 2019;39:23-7.  Back to cited text no. 4
Malmqvist L, Bursztyn L, Costello F, Digre K, Fraser JA, Fraser C, et al. The optic disc drusen studies consortium recommendations for diagnosis of optic disc drusen using optical coherence tomography. J Neuroophthalmol 2018;38:299-307.  Back to cited text no. 5
Borruat FX, Sanders MD. [Vascular anomalies and complications of optic nerve drusen]. Klin Monbl Augenheilkd 1996;208:294-6.  Back to cited text no. 6
Purvin V, King R, Kawasaki A, Yee R. Anterior ischemic optic neuropathy in eyes with optic disc drusen. Arch Ophthalmol 2004;122:48-53.  Back to cited text no. 7
Roh S, Noecker RJ, Schuman JS, Hedges TR 3rd, Weiter JJ, Mattox C. Effect of optic nerve head drusen on nerve fiber layer thickness. Ophthalmology 1998;105:878-85.  Back to cited text no. 8
Gittinger JW Jr, Lessell S, Bondar RL. Ischemic optic neuropathy associated with optic disc drusen. J Clin Neuroophthalmol 1984;4:79-84.  Back to cited text no. 9


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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