Clinical and Experimental Optometry | 2019
Reduced vision in a diabetic patient due to incidental leukaemic retinopathy
Abstract
A 55-year-old diabetic man was referred to the casualty eye service by his general medical practitioner with reduced vision for the past three weeks. It was questioned whether the diabetic condition of the patient could be related to his visual symptoms. The patient reported that his right eye had poor vision since childhood (possible diagnosis of amblyopia) and that over the past three weeks, the vision in his fellow eye did not feel as ‘sharp’ as it used to be. There were no other associated ocular or systemic symptoms. The past medical history of the patient included insulin-dependent type 2 diabetes mellitus, with erratic blood glucose control, hypertension and psoriasis. The patient reported that he had recently attended his annual diabetic retinopathy screening test, which resulted in a referral to the hospital eye service for referable retinopathy. Presenting visual acuity using the logMAR chart was less than 1.0 on the right eye and 0.58 on the left (equivalent to less than 6/60 in the right eye and approximately 6/24 in the left eye, when converted into Snellen acuity). Intraocular pressures were normal. Anterior segment examination revealed bilateral early nuclear sclerosis. Both of his anterior chambers and vitreous cavities were quiet. Dilated fundoscopy was in keeping with bilateral multiple retinal nerve fibre layer haemorrhages, occasional blot haemorrhages and cotton wool spots. There was also bilateral macular oedema, which was confirmed with macular optical coherence tomography. The retinal vessels were noted to be slightly tortuous. Fundus appearances are shown in Figures 1 and 2. The casualty officer examining the patient made the provisional differential diagnoses of severe pre-proliferative diabetic retinopathy with significant bilateral macular oedema or bilateral central retinal vein occlusions or hypertensive retinopathy. Given the severity of the retinal haemorrhages and the possibility of bilateral central retinal vein occlusions, a blood pressure check was ordered along with a blood workup including full blood count, urea and electrolytes, lipid profile and glucose. Blood pressure was normal. The blood results showed marked leukocytosis with white blood cells of 183.4 10/L (normal range 3.7–9.5 10/L). Haemoglobin was 104 g/L (normal range 133–176 g/L), platelets were 209 10/L (normal range 150–400 10/L) and glucose was 24 mmol/L (normal range 3.3–7 6 mmol/L). Urea and electrolytes and lipids were within normal ranges. A blood film was performed and it was commented that appearances were in keeping with chronic myeloid leukaemia. Given the markedly elevated white blood cell count, an urgent referral was made to the haematology department and the patient was admitted for further investigations. Given the suspicion of chronic myeloid leukaemia based on the blood film appearances, a bone marrow biopsy was performed which confirmed the diagnosis. Subsequently, leukopheresis was performed followed by administration of hydroxycarbamide and allopurinol. Targeted therapy using imatinib (a selective tyrosine kinase inhibitor) was also started to which the patient has responded well. He has since remained under ongoing review by the haematology team. With respect to his ocular management, after two weeks of observation without any improvement in the macular oedema following leukapheresis, the patient had an intravitreal dexamethasone 0.7 mg steroid implant (Ozurdex, Allergan) in his left eye, as there was no consensus between this or anti-vascular endothelial growth factor, given the underlying pathology. His right eye was not treated in the first instance as it was likely densely amblyopic. The intravitreal steroid implant resulted in the reduction of the macular oedema and the improvement of his visual acuity to 6/12 (from 6/24) at four weeks of follow-up. Two months following the Ozurdex implantation, the patient was switched to intravitreal aflibercept (Eylea, Bayer) on a three monthly basis as neovascularisation was now noted. His visual acuity continued to be stable between 6/9 and 6/12. The patient was nontolerant of the frequent anti-vascular endothelial growth factor injections and was therefore switched back to intravitreal steroid implants as required. Pan-retinal photocoagulation was performed and he has maintained a visual acuity of 6/7.5 to date in the 18 months of follow-up. With respect to his right eye, the patient developed neovascularisation of the disc and anti-vascular endothelial growth factor treatment using intravitreal aflibercept was