Delayed Non-arteritic Anterior Isch-emic Optic Neuropathy Following Acute Primary Angle Closure

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Delayed Non-arteritic Anterior Isch- emic Optic Neuropathy Following Acute Primary Angle Closure

Dear Editor,

Non-arteritic anterior ischemic optic neuropathy (NAION) secondary to acute primary angle closure (APAC) is a rare clinical disorder that leads to significant visual impairment. Although a number of cases of APAC-associated NAION have been reported, most in- volved NAION concurrent with APAC rather than second- ary to it [1-3]. Herein, we report a case of three-day-de- layed-onset NAION following APAC. We believe that this case illustrates the predispositional mechanism of post- APAC NAION occurrence.

A 64-year-old woman presented with two-day painful visual loss in the left eye. She had been diagnosed with systemic hypertension on a recent regular check-up. Visual acuity was 6 / 200 in the left eye and 20 / 25 in the right eye. Intraocular pressure (IOP) was 64 mmHg in the left eye and 15 mmHg in the right eye. There were signs of APAC in her left eye, including corneal edema, dilated and nearly-fixed pupil, and shallow anterior chamber. Optic disc exam revealed a hyperemic left optic nerve head (ONH) (Fig. 1A). Optical coherence tomography revealed slight inferior ONH swelling and inferior retinal nerve fi- ber layer (RNFL) edema (Fig. 1B). There was no relative afferent pupillary defect in either eye on swinging-light test. The patient was administered IOP-lowering and miot- ic medications, which reduced the left-eye IOP to 16 mmHg. Subsequently, laser iridotomy was performed without complication. The following day, the left eye visu- al acuity was 16 / 20, and the IOP was 16 mmHg. Coinci- dentally, the patient was examined using 24-hour ambula- tory blood pressure monitoring (already planned by the Internal Medicine physician) one day after APAC relief.

The results showed no significant systemic hypotension or nocturnal blood pressure dip. Three days later, however, painless left-eye vision loss was experienced upon waking in the morning. Visual acuity was 4 / 20, and IOP was 15 mmHg. The left pupil showed a relative afferent pupillary defect. The left ONH was diffusely swollen with disc hem-

orrhage at the temporal margin (Fig. 1C). Optical coher- ence tomography showed aggravated edema of the inferior RNFL (Fig. 1D). A Humphrey visual-field test showed a superior altitudinal visual-field defect corresponding to the inferior RNFL swelling (Fig. 1E). Based on these findings, left NAION was diagnosed. One year later, the left visual acuity was 16 / 20, and the IOP was 17 mmHg. The optic nerve edema of the left eye had subsided (Fig. 1F), but the RNFL showed atrophy (Fig. 1G). The visual-field defect was incompletely improved (Fig. 1H).

NAION is caused by hypo-perfusion of the ONH. Ocu- lar perfusion pressure is determined according to the dif- ference between mean arterial pressure and IOP. There- fore, NAION can develop in set tings of hemodynamic compromise such as systemic hy potension, blood loss, and anemia [4]. However, our patient showed no significant systemic hypotension or nocturnal blood pressure dip. In the present case, a significant increase in IOP reduced the perfusion pressure on the optic nerve due to compression of vessels in the prelaminar region [5].

ONH edema is a sign integral to the diagnosis of NAION. Patients with APAC sometimes also develop mild optic nerve edema that is not associated with NAION.

However, these cases can be differentiated from post- APAC NAION by the absence of subsequent optic nerve atrophy and preservation of visual acuity and the visual field [6].

According to our research, there have been no more than several case reports of NAION occurring simultaneously with APAC [1-3]. These reports posited only a possible as- sociation between APAC and NAION, and, when consid- ering that hypothesis, could not draw any firm conclusions as to whether APAC is a cause or a result. We believe that APAC is one of the possible causes of NAION. We suggest that slight but critical ONH edema (of the inferior portion in our case) caused by APAC-coincident ischemia initiates the vicious cycle of ONH ischemia, swelling, capillary compression, and additional ischemia, though we do not yet know the critical amount of optic-disc edema causing NAION. Additionally, premonitory ONH swelling is a well-recognized phenomenon in typical NAION [7].

Our present case demonstrates the possibility of the oc- currence of NAION despite successful APAC treatment and recovery of normal visual acuity. Therefore, close ob- servation of APAC with ONH edema is recommended.

Korean J Ophthalmol 2015;29(3):209-211

http://dx.doi.org/10.3341/kjo.2015.29.3.209

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210 Korean J Ophthalmol Vol.29, No.3, 2015

Kyoung Nam Kim

Department of Ophthalmology, Chungnam National University Hospital, Daejeon, Korea

Chang-Sik Kim, Sung Bok Lee, Yeon Hee Lee

Department of Ophthalmology, Chungnam National University Hospital, Chungnam National University College of Medicine, Daejeon, Korea

E-mail (Yeon Hee Lee): [email protected]

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

References

1. Nahum Y, Newman H, Kurtz S, Rachmiel R. Nonarteritic anterior ischemic optic neuropathy in a patient with prima- Fig. 1. Disc photographs and printout of optical coherence tomog- raphy (OCT) taken at the time of left acute primary angle closure show a hyperemic and slightly edematous left optic nerve head (A) and a slight inferior neuro-retinal rim edema and inferior retinal nerve fiber layer (RNFL) edema (B, black arrows). Three days af- ter angle closure relief (C,D,E), disc photograph shows a diffusely swollen optic nerve head with disc hemorrhage at the temporal mar- gin. The inferior pole is more swollen (C). OCT shows a diffusely, especially inferiorly, swollen RNFL (D, black arrow). Humphrey vi- sual field test demonstrates a superior altitudinal visual-field defect corresponding to inferior RNFL swelling (E). One year later, optic nerve head edema of the left eye subside (F). OCT shows RNFL thinning (G). The visual-field defect is only incompletely improved (H). OD = right eye; OS = left eye; TEMP = temporal; SUP = supe- rior; NAS = nasal; INF = inferior; VFI = visual field index; MD = mean deviation; PSD = pattern standard deviation.

800 400 0 0

Neuro-retinal rim thickness μm

TEMP SUP NAS INF TEMP

800 400 0 0

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP 800

400 0 0

11 18

3

<0 2

8 20 16

<0

8 5 7 12 18 21

<0

4 3 4 5 13 10 6 4 4 15 20

30 2118 30

15 23 25 21 24 24 25 21 25 25 25 25 15 15 0 23 18 26 25 24 24 27 24 23 23

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

VFI MDPSD

65%

-14.40 dB p < 0.5%

8.68 dB p < 0.5%

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

19 21

14 0 <0 18

21 19

<0

11 14 18 20 20 21

17 11 12 26 13 14 20 25 10 8 7 27

30 2013 30

14 20 23 17 21 22 20 17 24 23 20 19 18 24

<0

22 20 25 23 23 19 27 26 19 15

VFI MDPSD

80%

-11.50 dB p < 0.5%

5.96 dB p < 0.5%

0 30 60 90 120 150 180 210 240

OD OS

A B

800 400

0 0

Neuro-retinal rim thickness

μm

800 400

0 0

Neuro-retinal rim thickness

μm

0 30 60 90 120 150 180 210 240

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP 800

400 0 0

Neuro-retinal rim thickness

μm

11 18

3

<0 2

8 20 16

<0

8 5 7 12 18 21

<0

4 3 4 5 13 10 6 4 4 15 20

30 18 30

21 15 23 25 21 24 24 25 21 25 25 25 25 15 15 0 23 18 26 25 24 24 27 24 23 23

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

VFI MDPSD

65%

-14.40 dB p < 0.5%

8.68 dB p < 0.5%

0 30 60 90 120 150 180 210 240

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

19 21

14 0 <0 18

21 19

<0

11 14 18 20 20 21

17 11 12 26 13 14 20 25 10

8 7 27

30 13 30

20 14 20 23 17 21 22 20 17 24 23 20 19 18 24

<0

22 20 25 23 23 19 27 26 19 15

VFI MDPSD

80%

-11.50 dB p < 0.5%

5.96 dB p < 0.5%

0 30 60 90 120 150 180 210 240

OD OS

800 400 0 0

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP 800

400 0 0

11 18

3

<0 2

8 20 16

<0

8 5 7 12 18 21

<0

4 3 4 5 13 10 6 4 4 15 20

30 2118 30

15 23 25 21 24 24 25 21 25 25 25 25 15 15 0 23 18 26 25 24 24 27 24 23 23

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

VFI MDPSD

65%

-14.40 dB p < 0.5%

8.68 dB p < 0.5%

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

19 21

14 0 <0 18

21 19

<0

11 14 18 20 20 21

17 11 12 26 13 14 20 25 10 8 7 27

30 2013 30

14 20 23 17 21 22 20 17 24 23 20 19 18 24

<0

22 20 25 23 23 19 27 26 19 15

VFI MDPSD

80%

-11.50 dB p < 0.5%

5.96 dB p < 0.5%

0 30 60 90 120 150 180 210 240

OD OS

800 400 0 0

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP 800

400 0 0

11 18

3

<0 2

8 20 16

<0

8 5 7 12 18 21

<0

4 3 4 5 13 10 6 4 4 15 20

30 2118 30

15 23 25 21 24 24 25 21 25 25 25 25 15 15 0 23 18 26 25 24 24 27 24 23 23

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

VFI MDPSD

65%

-14.40 dB p < 0.5%

8.68 dB p < 0.5%

0 30 60 90 120 150 180 210 240 RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

19 21

14 0 <0 18

21 19

<0

11 14 18 20 20 21

17 11 12 26 13 14 20 25 10 8 7 27

30 2013 30

14 20 23 17 21 22 20 17 24 23 20 19 18 24

<0

22 20 25 23 23 19 27 26 19 15

VFI MDPSD

80%

-11.50 dB p < 0.5%

5.96 dB p < 0.5%

0 30 60 90 120 150 180 210 240

OD OS

E

H

C

F

D

G

800 400

0 0

Neuro-retinal rim thickness

μm

800 400

0 0

Neuro-retinal rim thickness

μm

0 30 60 90 120 150 180 210 240

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP 800

400 0 0

Neuro-retinal rim thickness

μm

11 18

3

<0 2

8 20 16

<0

8 5 7 12 18 21

<0

4 3 4 5 13 10 6 4 4 15 20

30 18 30

21 15 23 25 21 24 24 25 21 25 25 25 25 15 15 0 23 18 26 25 24 24 27 24 23 23

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

VFI MDPSD

65%

-14.40 dB p < 0.5%

8.68 dB p < 0.5%

0 30 60 90 120 150 180 210 240

RNFL thickness

SUP NAS INF TEMP

200 100 0 μm

TEMP

19 21

14 0 <0 18

21 19

<0

11 14 18 20 20 21

17 11 12 26 13 14 20 25 10

8 7 27

30 13 30

20 14 20 23 17 21 22 20 17 24 23 20 19 18 24

<⁰

22 20 25 23 23 19 27 26 19 15

VFI MDPSD

80%

-11.50 dB p < 0.5%

5.96 dB p < 0.5%

0 30 60 90 120 150 180 210 240

OD OS

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3. Kuriyan AE, Lam BL. Non-arteritic anterior ischemic op- tic neuropathy secondary to acute primary-angle closure.

Clin Ophthalmol 2013;7:1233-8.

4. Hayreh SS. Ischemic optic neuropathy. Prog Retin Eye Res 2009;28:34-62.

5. Hayreh SS. Blood supply of the optic nerve head and its role in optic atrophy, glaucoma, and oedema of the optic disc. Br J Ophthalmol 1969;53:721-48.

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Delayed Non-arteritic Anterior Isch-emic Optic Neuropathy Following Acute Primary Angle Closure

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