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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2002  |  Volume : 13  |  Issue : 1  |  Page : 45-49
Visual Loss in Uremic Patients on Dialysis: A Case Report and Review of Literature

Department of Nephrology, Jeddah Kidney Center, King Fahd Hospital, Jeddah, Saudi Arabia

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We report a 40-year-old female patient who was on maintenance hemodialysis for end-stage renal disease. She was initially noted to have severe hypertension necessitating use of four anti-hypertensive drugs. Gradually, and with regular dialysis, her blood pressure normalized without any medications, and subsequently she was noted to have pre- and post-dialysis blood pressure respectively of 90/60 mm Hg and 70/40 mm Hg which was asymptomatic. Following one session of dialysis during which she had severe hypotension associated with dizziness and headache, corrected by saline infusion, she noticed loss of vision affecting both eyes. Detailed evaluation including fundoscopy, magnetic resonance imaging, fluorescein angiography, color doppler and electroretinogram was performed. Empirical treatment with pulse methyl prednisolone and plasma exchange did not help. A diagnosis of anterior ischemia optic neuropathy due to hypotension was arrived at. Our case suggests that intra-dialytic hypotension can be problematic and should be treated aggressively.

Keywords: Hemodialysis, Hypotension, Visual loss, Ischemic optic neuropathy.

How to cite this article:
Basri NA, Shaheen FA. Visual Loss in Uremic Patients on Dialysis: A Case Report and Review of Literature. Saudi J Kidney Dis Transpl 2002;13:45-9

How to cite this URL:
Basri NA, Shaheen FA. Visual Loss in Uremic Patients on Dialysis: A Case Report and Review of Literature. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2021 Apr 14];13:45-9. Available from: https://www.sjkdt.org/text.asp?2002/13/1/45/33201

   Introduction Top

Ischemic optic neuropathy in its arteritic and non-arteritic varieties, causing visual loss has been reported in patients with renal failure. Most of the cases of ischemic optic neuropathy reported in the medical literature have been induced by shock. [1] The role of hypotension in the pathogenesis of idiopathic, non-arteritic anterior ischemic optic neuropathy (AION) is not clear. Hypotension during hemodialysis (HD) is the most frequent complication encountered in a dialysis unit and is considered the causative factor for ischemic optic neuro­pathy in uremic patients. [2]

   Case report Top

A 40-year-old woman with end-stage renal disease of unknown etiology was on maintenance HD from the age of 24 years. After one year on HD, she received a cadaveric renal transplantation in the United States and was on triple immunosuppresive medications (prednisolone, azathioprine and cyclosporine). She had two pregnancies post-renal transplantation; the first, six years after transplantation which ended by delivery of a full term normal baby boy, and the second, one year later, which ended by abortion in the first trimester. She was observed to have gradual deterioration of her renal graft functions which was histolo­gically proved to be chronic graft rejection with resultant loss of graft function nine years post-transplantation. She was then resumed on regular three times weekly HD sessions. During HD she used to have severe hypertension not responding to adjustment of volume status and neccessitating four different anti-hypertensive medications. One year after starting HD it was noticed that her blood pressure normalized without any medications and at a later stage, she was noticed to have chronic systemic hypo­tension. Pre-dialysis and post-dialysis blood pressures averaged 96/60 mm Hg and 70/40 mm Hg respectively. For more than two years on HD she had the same range of blood pressure which was not associated with any symptoms and was not responding to aggressive intra-dialysis therapy with isotonic saline, albumin, mannitol and dialysis against bicarbonate bath.

She presented to one such session of HD, with pre-dialysis blood pressure and pulse rate of 96/60 mm Hg and 90 beats/min respectively, and with 2.7 kgm increase in body weight above her dry weight. During the first three hours of dialysis, the vital signs remained unchanged. In the last hour of HD, her blood pressure dropped to 70/40 mm Hg and pulse rate was 100/min; she complained of mild dizziness and headache. Two hundred milliliters of normal saline were administered and blood pressure rose to 80/46 mm Hg and pulse rate was 92/min. The HD session was completed and the patient went home without any obvious discomfort. Six hours later, she noticed blurring of vision in both eyes, followed two hours later by complete loss of vision in the right eye. Eight hours later she developed loss of vision in the left eye also. She presented to us the following day with complete bilateral visual loss and a short report from an opthalmologist diagnosing the case as giant-cell arteritis. On the day of admission, she complained of inability to see any object or light and denied having focal or throbbing headache. Her blood pressure was 90/60 mm Hg and pulse rate 90 beats/min. Neurological examination was normal. Temporal arteries were not palpable or tender. Opthalmological examination revealed no light perception, fixed dilated pupils and normal extra-ocular muscle movement. Fundoscopic examination showed pale ischemic discs which were edematous with indistinct margins, edema of the macular area and patent central retinal arteries. Her hemoglobin was 74 g/l and erythrocyte sedimentation rate was 60 mm/hr. Biochemical tests showed a blood urea level of 43.2 mmol/L (60 mg/dl), sodium 142 mmol/L, potassium 5.8 mmol/L and glucose 5.04 mmol/L (90 mg/dl). An echocardiogram did not reveal any abnormality. Brain computed tomography was normal and magnetic resonance imaging of the brain showed abnormal hyper-intense signal in the white matter of the parito-occipital region bilaterally. Based on the clinical course, fundoscopic exami­nation and absence of cardiovascular and collagen disease, anterior ischemic optic neuropathy (AION) secondary to hypotension was diagnosed by two opthalmologists and a neurologist. Treatment was initiated with pulse therapy using 1 gm methyl pred­nisolone given daily for five days, followed by oral steroids, heparin and five sessions of 2 liters daily plasma exchanges. Routine dialysis was continued and she was given two units of packed red blood cells to maximize oxygen delivery. During hospita­lization her blood pressure was in the same range as earlier; 80-90/50-60 mm Hg. Despite all these measures, she did not show any improvement in vision. A second opinion from another opthalmologist at a specialized hospital was sought. She underwent some investigations including fundus fluorescein angiogram, bilateral colour doppler study, cerebral angiogram and electroretinogram all of which were normal. All these findings further suggested that she had ischemic optic atrophy with irreversible loss of vision.

   Discussion Top

Intra-dialytic hypotension is the most frequent complication of dialysis, occurring in 10 to 50% of all dialysis sessions. [2] The pathophysiology of hypotension in dialysis is multifactorial and most cases are ascribed to excessive volume, or rate of ultra­filtration. Autonomic nervous system dysfunction is common among patients undergoing dialysis and contributes to the pathogenesis of HD-induced hypotension. [3],[4],[5]

A number of additional factors contribute to intra-dialytic hypotension including declining serum osmolality associated with a hypotonic dialysate, the choice of acetate dialysate as well as the use of the conventional dialysate temperature of 37o C. Dialysis-induced hypotension usually causes mild and reversible symptoms such as dizziness, muscle cramps, nausea or light headedness. [4]

Our patient had dialysis-associated hypo­tension resulting in sudden, painless loss of vision as a presentation of AION. Anterior ischemic optic neuropathy is a clinical diagnosis, made on the findings of optic disc edema and a visual field defect in the setting of a history of sudden painless visual loss. [6] The pathogenesis of AION primarily involves interference with the posterior ciliary artery blood supply to the prelaminar optic nerve. [7] Risk factors predisposing to AION are decreased blood delivery (shock state), increased resistance to blood supply (hypertension and atherosclerosis) and low blood oxygen carrying capacity (anemia). [1] Our patient did not have symptoms of giant­cell arteritis, polyarteritis nodosa or systemic lupus erythomatosus which are well recognized causes of the arteritic form of AION. Giant-cell arteritis and optic neuritis were suspected by an opthalmologist in view of the overlap in the clinical profiles of optic neuritis and non-arteritic ischemic optic neuropathy. [8],[9] She received treatment with high-dose systemic steroids and plasmapheresis without response. Thus, a diagnosis of non-arteritic AION induced by hypotension during HD was made in our patient.

Various authors have documented an association between AION and severe hypo­tension. Many cases have occurred in patients with shock caused by massive hemorrhage during major surgery, cardiac arrest, gastro­intestinal haemorrhage or following cardiopulmonary bypass surgery. [10],[11],[12],[13],[14] Ischemic optic neuropathy in the setting of acute hypotension in uremic patients has been reported in association with other risk factors such as chronic hypertension, atherosclerosis and anemia. The suscep­tibility of the optic nerves to ischemia in patients with renal failure has been well documented. [15] The painless visual loss in these patients is related to optic disc edema from uremia and sometimes it mandates initiation of dialysis. [16]

Although numerous cases of ischemic optic neuropathy induced by shock have been reported in the medical literature, [10],[12],[17] the number of reports of ischemic optic neuro­pathy induced by hypotension in uremic patients are very few. Our patient represents a case of AION secondary to hypotension during HD similar to the case reported by Karen et al. [18] Haider and associates described four dialysis patients who developed typical non-arteritic AION. [19] Only one of their patients developed AION secondary to hypotension during HD while the other three had other risk factors beside being uremic including anemia, pre-existing hypertension and atherosclerosis. Aggressive early intervention to restore homeostasis by increasing the blood pressure or the hematocrit level resulted in partial recovery of vision in all the three uremic patients of Connolly who developed AION in the setting of acute hypotension. [20] More recently, another case of AION after hypotension during HD has been reported in conjunction with a case of hypotension related to massive gastrointestinal bleeding. [21]

The optic nerve head acquires a brittle intolerance to sudden fluctuations in systemic blood pressure because of impaired auto­regulation in case of chronic hypertension. Thus, relative hypotension during HD or during rapid correction of malignant hypertension may induce AION. [20],[22]

There is no reliable and effective treatment of AION. The efficacy of systemic steroid administration in the non-arteritic cases is debatable. [23] Our patient received high-dose steroids in the hope of decreasing optic disc edema and increasing blood flow to the optic nerve.[ 18],[23] Other forms of therapy have been tried including osmotic diuretics, hemodilution and surgical decompression of the optic nerve. Norepinephrine infusion when started early in normotensive patients, [24] or in patients who became hypotensive during rapid correction of malignant hypertension [20] resulted in improvement in visual acuity. Aspirin has shown a possible short-term, but little long-term, benefit in reducing the risk of non-arteritic AION. [25] Levodopa given to patients with recent­ onset non-arteritic AION appears to be beneficial. [26]

We conclude that, chronic HD patients who develop hypotension deserve aggressive measures to overcome this common complication which may rarely induce AION and catastrophic visual loss.

   References Top

1.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. 1    
2.Orofino L, Marcen R, Quereda C, et al. Epidemiology of symptomatic hypotension in hemodialysis: is cool dialysate bene­ficial for all patients? Am J Nephrol 1990;10:177-80.  Back to cited text no. 2    
3.Kersh ES, Kronfield SJ, Unger A, et al. Autonomic insufficiency in uremia as a cause of hemodialysis-induced hypo­tension. N Engl J Med 1974;290:650-3.  Back to cited text no. 3  [PUBMED]  
4.Henderson LW. Symptomatic hypotension during hemodialysis. Kidney Int 1980; 17:571-6.  Back to cited text no. 4  [PUBMED]  
5.Heidbreder E, Schafferhans K, Heidland A. Disturbances of peripheral and autonomic nervous system in chronic renal failure: effects of hemodialysis and transplantation. Clin Nephrol 1985;23:222-8.  Back to cited text no. 5  [PUBMED]  
6.Repka MX, Savino PJ, Schatz NJ, Sergott RC. Clinical profile and long term impli­cations of anterior ischemic optic neuro­pathy. Am J Opthalmol 1983;96:478-83.  Back to cited text no. 6    
7.Hayreh SS. Anterior ischemic optic neuro­ pathy. Br J Opthalmol 1974;58:955-89.  Back to cited text no. 7    
8.Rizzo III JF, Lessell S. Optic neuritis and ischemic optic neuropathy: Overlapping clinical profiles. Arch Opthalmol 1991; 109:1668-72.  Back to cited text no. 8    
9.Warner JE, Lessell S, Rizzo JF 3rd, Newman NJ. Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis? Arch Ophthalmol 1997; 115(11):1408-10.  Back to cited text no. 9    
10.Drance SM, Morgan RW, Sweeney VP. Shock-induced optic neuropathy: a cause of non progressive glaucoma. N Engl J Med 1973;288:392-5.  Back to cited text no. 10  [PUBMED]  
11.Rizzo JF 3rd, Lessell S. Posterior ischemic optic neuropathy during general surgery. Am J Ophthalmol 1987;103:808-11.  Back to cited text no. 11    
12.Johnson MW, Kincaid MC, Trobe JD. Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension. Opthal­mology 1987;94:1577-84.  Back to cited text no. 12    
13.Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982;32:560-2.  Back to cited text no. 13  [PUBMED]  
14.Busch T, Sirbu H, Aleksic I, et al. Anterior ischemic optic neuropathy: a complication after extracorporal circulation. Ann Thorac Cardiovasc Surg 1998;4(6):354-8.  Back to cited text no. 14    
15.Hamed LM, Winward KE, Glaser JS, Schatz NJ. Optic neuropathy in uremia. Am J Ophthalmol 1989;108:30-5.  Back to cited text no. 15  [PUBMED]  
16.Korzets Z, Zeltzer E, Rathaus M, Manor R, Bernheim J. Uremic optic nueropathy. A uremic manifestation mandating dialysis. Am J Nephrol 1998;18(3):240-2.  Back to cited text no. 16    
17.Hayreh SS. Anterior ischemic optic neuro­pathy. VIII. Clinical features and patho­genesis of post-hemorrhagic amaurosis. Ophthalmology 1987;94:1488-502.  Back to cited text no. 17    
18.Servilla KS, Groggel GC. Anterior ischemic optic neuropthy as a complication of hemo­dialysis. Am J Kidney Dis 1986;8:61-3.  Back to cited text no. 18  [PUBMED]  
19.Haider S, Astbury NJ, Hamilton DV. Optic nueropathy in uraemic patients on dialysis. Eye 1993;7(1)148-51.  Back to cited text no. 19    
20.Connolly SE, Gordon KB, Horton JC. Salvage of vision after hypotension induced ischemic optic neuropthy. Am J Ophthalmol 1994;117:235-42.  Back to cited text no. 20  [PUBMED]  
21.Koos MJ, Munteanu G. Anterior ischemic optic neuropathy after systemic hypo­tension and anemia. Oftalmologia 1998; 44(3):79-83-60.  Back to cited text no. 21    
22.Taylor D, Ramsay J, Day S, Dillon M. Infarction of the optic nerve head in children with accelerated hypertension. Br J Ophthalmol 1981;65:153.  Back to cited text no. 22  [PUBMED]  
23.Shults WT. Ischemic optic neuropathy. Still the ophthalmologist dilemma. Oph­thalmology 1984;91(11)1338-41.  Back to cited text no. 23    
24.Kollarits CR, McCarthy RW, Corrie WS, Swann ER. Norepinephrine therapy of ischemic optic neuropathy. J Clin Neuro­ophthalmol 1981;1(4):283-8.  Back to cited text no. 24    
25.Beck RW, Hayreh SS, Podhajsky PA, Tan ES, Moke PS. Aspirin therapy in non­arteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123(2):212-7.  Back to cited text no. 25    
26.Johnson LN, Guy ME, Krohel GB, Madson RW. Levodopa may improve vision loss in recent-onset, nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2000; 107:521-6.  Back to cited text no. 26    

Correspondence Address:
Faissal AM Shaheen
Consultant Physician & Nephrologist, Saudi Center for Organ Transplantation, P.O. Box 27049, Riyadh 11417
Saudi Arabia
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PMID: 18209412

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