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Year : 2013  |  Volume : 6  |  Issue : 1  |  Page : 64-65  

Anterior ischemic optic neuropathy and dialysis: Effect of hypotension

Department of Ophthalmology, Sultan Qaboos University Hospital, Muscat, Oman

Date of Web Publication15-May-2013

Correspondence Address:
Buthaina I Sabt
Department of Ophthalmology, Sultan Qaboos University Hospital, Muscat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-620X.111934

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How to cite this article:
Sabt BI. Anterior ischemic optic neuropathy and dialysis: Effect of hypotension. Oman J Ophthalmol 2013;6:64-5

How to cite this URL:
Sabt BI. Anterior ischemic optic neuropathy and dialysis: Effect of hypotension. Oman J Ophthalmol [serial online] 2013 [cited 2022 Jan 23];6:64-5. Available from: https://www.ojoonline.org/text.asp?2013/6/1/64/111934


Nonarteritic anterior ischemic optic neuropathy (NAION) is known to be the most common acute optic neuropathy in patients aged over 50 years [1] with fellow eye involvement in 15% of patients at 5 years. [2] Bilateral, simultaneous anterior ischemic optic neuropathy (AION) is a rare presentation and is frequently associated with severe hypotension. [3] We present three patients of NAION in patients undergoing dialysis to highlight the role of hypotension and its effects on the optic nerve.

   Patient 1 Top

A 24-year-old female presented with sudden loss of vision in her left eye (OS). Her past medical history was significant for chronic renal failure secondary to chronic reflux as a child, one previous failed renal transplant and dialysis four times a week. She used to complain of severe ocular pain in both eyes (OU) during dialysis, which was attributed to repeated episodes of systemic hypotension, which aggravated ocular ischemia. Due to this she was put on home oxygen 100% 24 hours a day and this significantly improved her pain, which was felt to be coming from an ocular ischemic syndrome.

She was diagnosed to have left posterior ION and bilateral ocular ischemic syndrome with rubiosis iridis. She underwent pan retinal photocoagulation (PRP) and intravitreal injection of Avastin®. This had no effect on vision and the rubeosis iridis, but did reduce the new vessels in the retina. Two months later she presented with a painful right AION. She then developed a right posterior subcapsular cataract and her vision dropped to hand movements. Her cataract was removed and her vision improved to 6/60. However, one month later she developed a right recurrent ION affecting the inferior arcade and hence she lost her superior field of vision. The patient died 3 months after her cataract surgery due to complications of chronic renal failure.

   Patient 2 Top

A 30-year-old female presented with sudden loss of vision OS. Past medical history was significant for renal failure secondary to glomerulonephritis and she was on dialysis while waiting for renal transplantation. She too was experiencing low blood pressure during dialysis. She was found to have a left posterior ION with a superior altitudinal defect on Goldmann visual field testing. She represented 3 months later with loss of residual inferior field OS. Six months after her initial presentation with visual loss, she suffered a right AION affecting the inferior part of the annulus and causing a right superior field defect. She also developed mild ocular ischemic syndrome with a right cataract for which she underwent a right phacoemulsifcation and intraocular lens implantation (IOL). She has maintained vision of 6/9 OD as she still has her inferior field and is under 6 monthly review.

   Patient 3 Top

A 72-year-old male on peritoneal dialysis for renal failure from chronic glomerulonephritis presented with sudden loss of vision OS. He had a left AION with an altitudinal field defect affecting the inferior part of this visual field. The ION was attributed to systemic hypotension associated with continuous peritoneal dialysis.

Nonarteritic AION presents as a sudden visual loss that many patients report on awakening, with an afferent pupillary defect and optic disc edema. Visual field analysis mostly shows nerve fiber bundle defects, mainly inferior altitudinal. AION is believed to occur due to interference with the posterior ciliary artery blood supply to the prelaminar optic nerve. Hayreh very importantly described nocturnal hypotension as the most important precipitating factor in the pathogenesis of AION in normal patients and it explains why patients with AION complain of visual loss on awakening. [4]

Patients under dialysis are generally prone to hypotensive events, which places them at risk for developing AION. [5],[6],[7] Jackson described ambulatory blood pressure monitoring in a patient undergoing peritoneal dialysis who suffered bilateral AION, showing severe drops in nocturnal blood pressure, with diastolic readings as low as 41 mmHg. [8]

One would expect that the continuous nature of peritoneal dialysis will place patients at a lower risk of systemic hypotension when compared with patients on hemodialysis. However, reports in literature are distributed equally into peritoneal and hemodialysis groups and clearly hypotension is the precipitating factor in both types of patients. [7],[8],[9],[10] Uremic patients often may also have other coexisting pathological factors such as hypotension (decreased blood delivery), or hypertension, atherosclerosis, and anemia (low blood oxygen carrying capacity), that predispose them to AION.

Systemic steroids has often been the mode of therapy in AION. But there is no strong evidence that favors their use. The rationale for use of steroids in NAION comes from the late 1960s that steroids would decrease capillary permeability, thereby inducing faster resolution of disc edema and this would reduce compression of capillaries in the optic nerve head and improve blood flow, restoring the function of surviving, but nonfunctioning, ischemic axons. NAION remains frustrating for clinicians and often devastating for patients. The pathophysiology remains unclear, and it is uncertain whether any treatment will be effective for NAION. The role of steroids remains controversial, and although steroids might accelerate resolution of disc edema, there is currently no evidence that a shorter duration of disc edema is associated with improved visual outcome. The controversy should be seen as stimulus to expand the research on the pathophysiology and treatment of NAION rather than proof that steroids are an effective treatment for acute NAION."

Therapy of AION related to dialysis is unsatisfactory. Conolly reported visual recovery in hypotensive AION following vigorous pressure rise. Hyperbaric oxygen therapy elevates the dissolved oxygen content of blood, thereby providing increased tissue oxygen and potentially reducing damage in injured axons. [11] The effect of hyperbaric oxygen in 20 nonarteritic AION patients between 3 and 20 days of onset of visual loss was evaluated. There was no improvement in visual acuity or visual field even in the subgroup treated within 9 days of onset of symptoms. [12]

Special attention should be given to patients undergoing chronic dialysis. Prevention of severe hypotensive events is very crucial in preventing potentially blinding condition. Once AION is established, treatment will probably be ineffective in restoring vision.

   Acknowledgment Top

The author gratefully acknowledges Prof. L. Cassidy, Consultant Neuro-ophthalmology and Oculoplasty, Royal Victoria Eye and Ear Hospital, Adelaide road, Dublin 2. The patients reported in this letter were drawn from her practice.

   References Top

1.Miller NR. Walsh and hoyt's clinical neuro-ophthalmology. 4 th ed. Vol. 1 . Baltimore: Williams and Wilkins; 1982. p. 219-21 .  Back to cited text no. 1
2.Newman NJ, Scherer R, Langenberg P, Kelman S, Feldon S, Kauman D, et al. The fellow eye in NAION: Report from the iscahemic optic neuropathy decompression trial follow up study. Am J Ophthalmol 2002;134:317-28.  Back to cited text no. 2
3.Basile C, Addabbo G, Montanaro A. Anterior ischaemic optic neuropathy: Role of hypotension and anaemia. J Nephrol 2001;14:420-3 .  Back to cited text no. 3
4.Hayreh S, Podhajsky P, Zimmerman MB. Role of nocturnal arterial hypotension in optic nerve head ischaemic disorders. Ophthalmologica 1999;213:76-96.  Back to cited text no. 4
5.Beri M, Klugman MR, Kohler JA, Hayreh SS. Anterior ischaemic optic neuropathy.VIII, Incidence of bilaterality and various influencing factors . Ophthalmology 1987;94;1020-8.  Back to cited text no. 5
6.Korzets A, Marashek I, Schwartz A, Rosenblatt I, Herman M, OriY. Ischaemic optic neuropathy in dialzed patients: A previously unrecognized manifestation of calcific uremic artriopathy. Am J Kidney Dis 2004;44:E93-7 .  Back to cited text no. 6
7.Servilla KS, Gorggel GC. Anterior ischaemic optic neuropathy as a complication of hemodialysis. Am J Kidney Dis 1986;8:61-3.  Back to cited text no. 7
8.Jackson TL, Farmer CK, Kingswood C, Vickers S . Hypotensive ischaemic optic neuropathy and peritoneal dialysis. Am J Ophthalmol 1999;128:109-11 .  Back to cited text no. 8
9.Buono LM, Foroozan R, Savino PJ, Danesh-Meyer HV, Stanescu D. Posterior ischemic optic neuropathy after hemodialysis. Ophthalmology 2003;110:1216-8.  Back to cited text no. 9
10.Nieto J, Zapata MA. Bilateral anterior ischemic optic neuropathy in patients on dialysis: A report of two cases. Indian J Nephrol 2010;20:48 - 50.  Back to cited text no. 10
11.Conolly SE, Gordan KB, Horten JC . Salvage of vision after hypotension-induced ischaemic optic neuropathy. Am J Ophthalmol 1994;117:235-42.  Back to cited text no. 11
12.Arnold AC, Helper RS, Lieber M, Alexander JM. hyperbaric oxygen therapy for nonarteritic anterior ischaemic optic neuropathy. Am J ophthalmol 1996;122:535-41.  Back to cited text no. 12

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