Bilateral macular infarction secondary to haemodialysis in a patient with chronic renal failure

Abstract

Improved management of patients who have end-stage renal disease and are dependent on haemodialysis (HD) have resulted in increased life expectancy.1 Patients with chronic renal failure and renal replacement therapy can have vision loss either due to primary disease as diabetic retinopathy and hypertension or secondary to complications associated with dialysis. HD can cause ocular vascular diseases such as ischaemic optic neuropathy and retinal vein occlusion which cause severe visual loss in patients with end-stage renal disease.2 However, no case of macular infarction post-HD has been reported to date. A 70-year-old man presented with sudden painless loss of vision in both eyes for 1 day. There was no history of trauma or other symptoms suggestive of cerebrovascular event. Systemically he was a known case of chronic renal insufficiency secondary to hypertension and was on renal replacement therapy for the last 6 months twice a week. He had undergone HD 1 day before and complaint of loss of vision immediately after the procedure. The patient was on erythropoietin and antihypertensive medication. There was no history of diabetes or any other systemic abnormality as coronary artery disease and cerebrovascular accident. The patient had visual acuity of finger counting close to face both eyes with projection of light present in all quadrants. On ophthalmological evaluation, anterior segment was normal with no evidence of neovascularization of iris. There was no evidence of disc oedema. There was grade II hypertensive retinopathy with arteriovenous ratio of 1:3 and arteriovenous crossing changes. Veins were not dilated and non-tortuous. There were scattered retinal haemorrhages without exudation at the posterior pole. However, macula appeared pale in both eyes with surrounding retinal opacification (Fig. 1a,b). Fundus photo of right (a) and left (b) eye showing diffuse retinal opacification. Fundus fluorescein angiography of right (c) and left (d) eye showing marked non-perfusion of the macula with non-filling of the macular arterioles. Optical coherence tomography of right (e) and left (f) eye showing elevated fovea with extensive cystic changes. Systemic parameters included blood pressure – 142/84 mmHg, haemoglobin – 10.4 gm%, platelets – 175 000/mm3, total leucocyte count – 9000/mm3, blood urea – 60 mg/dL, serum creatinine – 1.6 mg/dL. Fundus fluorescein angiography showed extensive macular ischaemia with non-filling of retinal arterioles with no leakage anywhere else (Fig. 1c,d). Optical coherence tomography showed extensive cystic changes in both eyes (Fig. 1e,f). The diagnosis of bilateral macular infarction secondary to hypotension post-HD was made. We explained about the irreversible nature of the condition to the patient and expressed our inability to administer any treatment as described in the literature. The patient came for a routine follow up after 4 weeks. The visual acuity and fundus picture was the same as it was at presentation. Macular infarction has been reported due to various other causes including sickle cell disease, vascular occlusion, diabetes, malignant hypertension, thrombotic thrombocytopenic purpura and secondary to aminoglycoside toxicity. However, macular infarction post-HD has never been reported. Post-HD hypotension and viscosity changes leading to macular infarction are postulated as probable cause of macular infarction.3 As blood flow through any tissue is inversely related to viscosity of blood (Poiseuille's law), HD decreases retinal blood flow by enhancing blood viscosity roughly equivalent to the volume of fluid removed in addition to an increase in haematocrit.4,5 The erythropoietin therapy, which the patient was on, also might have contributed to a higher haematocrit. The resultant diminished retinal circulation leads to bilateral macular ischaemia and infarction in this subject. As macula is supplied by long and thin capillaries with absent collateral circulation, it is highly predisposed to ischaemia in case of macular hypoperfusion as also is reported in patients with sickle cell disease. Macular ischaemia leads to fluid accumulation in inner retinal layers due to alteration in blood retinal barrier and thus produces cystic changes as also is evident in the optical coherence tomography of this subject (Fig. 1e,f). To the best of our knowledge, bilateral macular infarction secondary to HD has never been reported and is a serious irreversible complication.