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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 33  |  Issue : 3  |  Page : 353-355

A case of bilateral sequential optic neuropathy in a young adult post hemodialysis


Department of Ophthalmology, D Y Patil Medical College, Navi Mumbai, Maharashtra, India

Date of Submission11-Oct-2020
Date of Decision24-Oct-2020
Date of Acceptance25-Oct-2020
Date of Web Publication08-Dec-2021

Correspondence Address:
Dr. Harsha Sameer Pagad
D Y Patil Medical College, Nerul, Navi Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kjo.kjo_158_20

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  Abstract 


Ischemic optic neuropathy is a very rare but well-known complication following hemodialysis in patients with chronic kidney disease, It can be potentially blinding when involving both optic nerves and there is no effective established treatment available so far. If involvement of one eye is detected earlier, a multidisciplinary approach and efforts directed at controlling risk factors such as anemia and hypotension will go a long way in preventing the involvement of other eye in young individuals. We report a case of posterior ischemic optic neuropathy in the right eye with recovery of vision but persistent color vision deficit with recent-onset nonarteritic anterior ischemic optic neuropathy in the left eye, which has not been reported so far.

Keywords: Anemia, hemodialysis, hypotension, ischemic optic neuropathy, visual loss


How to cite this article:
Pagad HS, Hariyani R, Shanbhag NU. A case of bilateral sequential optic neuropathy in a young adult post hemodialysis. Kerala J Ophthalmol 2021;33:353-5

How to cite this URL:
Pagad HS, Hariyani R, Shanbhag NU. A case of bilateral sequential optic neuropathy in a young adult post hemodialysis. Kerala J Ophthalmol [serial online] 2021 [cited 2022 Jan 19];33:353-5. Available from: http://www.kjophthal.com/text.asp?2021/33/3/353/331929




  Introduction Top


As described in the literature, anterior ischemic optic neuropathy (AION) primarily involves interference with the posterior ciliary arterial blood supply to the prelaminar optic nerve.[1] This might be brought about by decreased blood delivery, increased resistance to blood supply, or low blood oxygen-carrying capacity.[2] Patients with chronic kidney disease have comorbidities such as hypertension, atherosclerosis, and anemia, which predispose them to ischemic optic neuropathy. An association between acute ischemic optic neuropathy and hypotension during general surgeries, cardiopulmonary bypass, has been documented in various case reports. Hemodialysis-associated hypotension has also been proven as a significant cause of ischemic optic neuropathy. We report one such unique case of old posterior ischemic optic neuropathy (PION) in one eye with sequential involvement of other eye in the form of nonarteritic anterior ischemic optic neuropathy (NAAION) in a young adult male on hemodialysis, which has not been reported before.


  Case Report Top


A 31-year-old male patient admitted in the medicine department was referred to our outpatient department with a history of sudden-onset painless decrease in vision in the left eye 15 days before following a session of hemodialysis. There were no history of redness, photophobia, and flashes/floaters; no associated pain on eye movements; and no history of headache, and vomiting. There was a history of a similar episode of diminution of vision in the right eye a year back with complete recovery in few weeks. The patient was a case of bilateral chronic kidney disease for the past 3 years. He was on dialysis for 2 years, thrice weekly, and on antihypertensive medications. No other significant past or family history was present.

Ocular examination revealed a visual acuity of 20/20 in the right eye and counting fingers at 3 m in the left eye, not improving with pinhole with Snellen's chart. Pupillary evaluation showed a briskly reacting pupil to light in the right eye and sluggishly reacting pupil in the left eye. There was Grade 1 relative afferent pupillary defect in the left eye. There was no light near dissociation. Extraocular movements were full in both eyes. There was no pain associated with eye movements. Color vision recorded with the Ishihara pseudoisochromatic chart was 1/16 in the right eye and 0/16 in the left eye. Intraocular pressure was within normal range in both eyes. Fundus examination with slit-lamp biomicroscopy of the right eye showed 0.3:1 cup-by-disc ratio with mild temporal pallor [Figure 1]. The left eye showed 0.3:1 cup-by-disc ratio, sectoral inferior pallid disc edema [Figure 2]. There was no evidence of any hemorrhages. Foveal reflex was present in both eyes, with the rest of the retinal examination being normal. Humphrey visual field automated perimetry 30-2 Swedish Interactive Threshold Algorithm (SITA) standard was done. The right eye showed peripheral constriction of fields on the nasal side [Figure 3] and the left eye showed incomplete biarcuate defects [Figure 4]. The patient was diagnosed as NAAION in the left eye and PION in the right eye based on the above findings. His blood reports showed high serum creatinine (9.3 mg/dL), serum urea (66.5 mg/dL), and blood urea nitrogen (31.07 mg/dL). His hemoglobin was 8.3 mg/dL, along with a low red blood cell count. Computed tomography scan brain with orbit was done, in which no significant abnormality was noted. The patient was advised to avoid antihypertensive medications in the evening to avoid nocturnal hypotension, and medications for correction of anemia were prescribed. The patient was followed up after 2 months. The visual acuity was the same and color vision was 1/16 in the right eye and 1/16 (from 0/16 previously) in the left eye. On dilated fundus examination, the left eye showed inferotemporal disc pallor with resolving disc edema.
Figure 1: Fundus photo of Right eye showing mild temporal pallor of disc

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Figure 2: Fundus photo of Left eye showing inferior pallid disc oedema

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Figure 3: Perimetry 30-2 of Right eye showing nasal constricted field

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Figure 4: Perimetry 30-2 of Right eye showing incomplete biarcuate defects, denser superiorly

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  Discussion Top


Optic nerve disease has been reported in patients with renal dysfunction. It was presumed to be due to uremia and hence toxic optic neuropathy. The incidence of optic neuropathy of renal failure has not been determined. Sajjad et al. observed four patients on dialysis with optic neuropathy. Each patient had long-standing renal failure and its sequelae of anemia and hypertension. The immediate causes of ischemia were hypotension in 1, severe anemia in 1, and generalized atherosclerosis in two patients.[3] Optic neuropathy is a well-known complication of renal failure/dialysis. A neurotoxic type of optic neuropathy in uremic patients with a serum urea nitrogen level of >35.7 mg/dl was reported by Knox et al., who implicated hypertension and anemia as well as a raised serum urea nitrogen. Medical management with hemodialysis was followed by improvement of vision in four of their patients.[4] Hamad et al. described a similar type of optic neuropathy in patients maintained on dialysis.[5] Karen et al. reported a case of AION as a result of hemodialysis-associated hypotension (decreased blood delivery).[6] The pathogenesis of AION primarily involves interference with the posterior ciliary artery blood supply to the prelaminar optic nerve.[7] This might be brought about by decreased blood delivery, increased resistance to blood supply, or low blood oxygen-carrying capacity.[8]

Uremic patients may often have coexisting pathology such as hypertension, atherosclerosis (increased resistance), and anemia (low blood oxygen-carrying capacity), predisposing them to ischemic optic neuropathy.[3] Systemic steroids have often been the mode of therapy in AION. However, there is no strong evidence that favors their use. The rationale for the use of steroids in NAAION 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.[9] Our patient had dialysis-associated hypotension and anemia, resulting in sudden painless loss of vision as a presentation of AION and PION, which was the diagnosis made by clinical correlation and perimetry findings. The patient improved along with the medical management of hypotension and anemia, which was seen on further follow-up visits. In conclusion, with the expansion of the demand for renal replacement therapy, an increasing number of patients are receiving dialysis, often in the presence of multiple pathologies, including diabetes, generalized atherosclerosis, and hypertension.[3] By identifying the risk factors and by ambulatory monitoring of blood pressure during dialysis, the occurrence of ischemic optic neuropathy can be prevented.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hayreh SS. Anterior ischaemic optic neuropathy. Br J Ophthalmol 1974;58:955-89.  Back to cited text no. 1
    
2.
Foulds W. Visual disturbance in systemic disorders: Optic neuropathy and systemic disease. Trans Ophthalmol Soc UK 1969;89:125-46.  Back to cited text no. 2
    
3.
Haider S, Astbury N, Hamilton D. Optic neuropathy in uraemic patients on dialysis. Eye 1993;7:148-51.  Back to cited text no. 3
    
4.
Knox DL, Hanneken AM, Miller NR, Gonzalea WL. Uraemic optic neuropathy. Arch Ophthalmol 1988;106:50-4.  Back to cited text no. 4
    
5.
Hamed LM, Winward KE, Glaser JS, Schatz NJ. Optic neuropathy in uremia. Am J Ophthalmol 1989;108:30-5.  Back to cited text no. 5
    
6.
Karen S, Servilla MD, Grogge GC. Anterior ischaemic optic neuropathy as a result of haemodialysis associated hypotension. Am J Kidney Dis 1986;8:61-3.  Back to cited text no. 6
    
7.
Hayreh SS. Anterior ischaemic optic neuropathy. Br J Ophthalmol 1974;58:955-89.  Back to cited text no. 7
    
8.
Foulds W. Visual disturbance in systemic disorders: Optic neuropathy and systemic disease. Trans Opthalmolol Soc UK 1969;89:125-46.  Back to cited text no. 8
    
9.
Sabt BI. Anterior ischemic optic neuropathy and dialysis: Effect of hypotension. Oman J Ophthalmol 2013;6:64-5.  Back to cited text no. 9
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