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Patterns of Visual Loss in Untreated Sickle Cell Retinopathy

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Patterns of Visual Loss in Untreated Sickle Cell Retinopathy Eye (1988) 2, 330-335 Patterns of Visual Loss In Untreated Sickle Cell Re­ tinopathy B J MORIARTY, R W ACHESON, P I CONDON and G R SERJEANT Jamaica Summary Ophthalmic assessments of 120 patients with homozygous sickle cell (SS) disease and of 222 with sickle cell haemoglobin-C (SC) disease were conducted over a period of ten years. Visual acuity loss (V.A.::S;6/18) attributable to sickle cell retinopathy occurred in 10% of untreated eyes during a mean observation period of 6.9 years. Visual loss was strongly associated with proliferative sickle retinopathy (p<O.OOI) and most commonly resulted from vitreous haemor­ rhage, tractional retinal detachment and epiretinal membranes. The incidence of visual loss was 31 per 1000 eye-years observation among eyes with proliferative disease compared to 1.4 per 1000 eye-years observation among eyes with non-proliferative disease. The natural history and ocular complications lusion of 16 eyes. Dense vitreous haemor­ of sickle cell retinopathy are extensively rhages prevented fundoscopy at the start of described,l-4 but little attention has been the study in 14 eyes but these eyes were focussed on the frequency or causes of visual included after spontaneous resolution of the loss associated with this condition. The pre­ haemorrhage. No eyes had received treat­ sent study describes visual loss in patients ment prior to entry into the study. The final with untreated sickle cell retinopathy and dis­ study group included 342 patients (120 SS, cusses the causes of visual morbidity. 222 SC) aged 15-60 years at enrolmenL The age and sex distribution of patients is sum­ Materials and Methods marised in Table 1. The average duration of Over 3000 patients have attended the sickle follow-up of patients was 6.9 years (Fig 1). cell clinic of the University Hospital of the Assessment included visual symptoms, West Indies or a group of periheral sickle cell corrected visual acuity, slit lamp biomicros­ clinics operated by staff of the Medical copy and intraocular pressure. Direct and Research Council Laboratories. This repre­ indirect ophthalmoscopy were carried out sents approximately one third of all after mydriasis. Red free and colour photo­ Jamaicans with sickling haemog­ graphy and fluorescein angiography were lobinopathies. performed where appropriate. The study group consisted of all those 'Moderate' visual loss was defined as best patients with SS or SC disease, aged 15 years corrected visual acuity of 6/18 - 6/60 and 'se­ and over who underwent ophthalmic screen­ vere' visual loss as best corrected visual ing on at least two occasions separated by 3 acuity <6/60, on at least two occasions sepa­ months or more during the 10 year period 1st rated by at least 3 months. Those eyes show­ October 1976 to 30th September 1986. ing 'severe' visual loss after a preceding Cataracts preventing fundoscopy caused exc- episode of 'moderate' visual loss (e.g. vitre- From: The Medical Research Council Laboratories (Jamaica), University of the West Indies, Kingston, Jamaica Correspondence to: B J Moriarty, MA(Cantab), FRCS, Moorficlds Eye Hospital, High Holborn, London WCl VISUAL LOSS IN UNTREATED SICKLE CELL RETINOPATHY 331 Table I Patients and eyes examined according to sex and age when last seen MALES FEMALES TOTAL AGE PATIENTS EYES PATIENTS EYES PATIENTS EYES 15-29 73 105 82 145 155(45%) 250(45%) 30-49 72 112 93 148 165(48%) 260(47%) 50+ 8 16 14 28 22( 7%) 44( 8%) TOTAL 153 233 189 321 342 554 (45%) (42%) (55%) (58%) ous haemorrhages, tractional retinal detach­ ment) were counted as 'severe'. If any eye developed proliferative changes after a pre­ ceding period of non-proliferative -retinopathy, the eye was classified as 'pro­ Potfenis liferative' and follow-up time was measured from the time of onset of proliferative dis­ ease. A randomised controlled trial of Xenon . 10 11 feeder coagulation of proliferative sickle Duration(yrsJ retinopathy (PSR5.6 conducted between 1978 Numbers and duration of patient follow up. and 1980 resulted in the treatment of 53 eyes Fig. 1. of 78 patients. A randomised controlled trial of Argon scatter photocoagulation conducted haemorrhage and traction retinal detachment since 1982 has resulted in the treatment on 61 (Table II). Analysis of 16 eyes with vitreous eyes of 67 patients. This report describes vis­ haemorrhages examined within two weeks of ual loss in the control eyes of these trials and onset of symptoms and observed over one in both eyes of all other patients where fun­ year indicated that first symptomatic doscopy was possible. haemorrhages were associated with transient « 3 months) and generally moderate visual Results loss whereas subsequent symptomatic Visual loss (V.A.� 6/18) occurred in 72 eyes haemorrhages generally caused prolonged during the study period. (> 3 months) and severe visual loss (Table In 52 (10%) eyes of 49 (15%) patients, this III). The commonest cause of visual loss was attributable to sickle cell retinopathy, among eyes without proliferative change was being associated with proliferative changes in angioid streaks and disciform degeneration 45 eyes and non-proliferative changes in 7 (Table IV). eyes. Visual loss was 'severe' in 27/52 (52%) In 20 eyes, visual loss was not attributable of eyes involved. The prevalence of visual to sickle cell disease but to cataract (8 eyes), loss was 45/134 (34%) among eyes affected glaucoma (5 eyes), uveitis (5 eyes), myopia by PSR which was significantly greater (X2 = and trauma (1 eye each). 114.2, p<O.OOl) than among the 7/420 (2%) eyes with non-proliferative disease. The inci­ Discussion dence of visual loss was 31 per 1000 eye-years There have been few assessments on the pre­ of observation among eyes affected by PSR valence of visual loss in patients with sickle compared to 1.4 per 1000 eye-years among cell disease. An earlier study3 described eyes with non-proliferative changes (X2 = severe visual loss in 12% of eyes with PSR 110.2, p<O.OOl) giving a relative risk of 23 over an average follow-up of 4 years but since (95% confidence interval = 8-66). eyes severely affected by PSR were enrolled The commonest causes of visual loss in a trial of Xenon arc photocoagulation,? among eyes affected by PSR were vitreous this may have underestimated the prevalence 332 B. J. MORIARTY ET AL. of visual loss among untreated patients. The demonstrated a higher prevalence of PSR in present study observed severe visual loss in the SC patients (32%) compared to SS 17% of PSR af£ected eyes over a mean fol­ patients (3% ).2,3 Screening of asymptomatic low-up period of 6.9 years. patients is biased towards SC patients. This is Earlier studies on non-selected patients reflected in the study group described, by the Table II Causes of 'moderate' and 'severe' visual loss in proliferative sickle retinopathy (Eyes) N= 134) 'MODERATE' 'SEVERE' TOTAL CAUSES Nos. (%) Nos. (%) Nos. (%) Vitreous haemorrhage 10 (46) 10 (43) 20 (44) Tractional retinal detachment 5 (23) 9 (39) 14 (31) Epiretinal membranes 6 (27) 2 ( 9) 8 (1 8) Mixed vitreous haemorrhage + traction detach. 2 ( 9) 2 ( 4) Rhegmatogenous retinal detachment ( 4) 1 ( 2) TOTAL 22 23 45 Table III Characteristics of first and subsequent vitreous haemorrhages (V.H.) First symptomatic v.H. Subsequent v.H. (N = 8) (N= 8) PSR > 60° 8 (100%) 8 (100%) SC Genotype 8 (1 00%) 8(100%) Visual loss > 3112 o 7 ( 88%) Severe visual loss within 2/52 2 ( 25%) 8 (100%) Complications o 8 (100%) Persistence of V.H. > 6/12 = 6 cases Traction detachment = 2 cases Table IV Causes of 'moderate' and 'severe' visual loss in non-proliferative sickle cell retinopathy (Eyes) (N = 420) TOTAL 'MODERATE' 'SEVERE' CAUSES Nos. Nos. Nos. (%) Angioid streaks with disciform degeneration 4 4 (57%) Sickling maculopathy 2 2 (29%) Branch retinal artery occlusion (14%) TOTAL 3 4 7 VISUAL LOSS IN UNTREATED SICKLE CELL RETINOPATHY 333 preponderance of SC patients (222) com­ detachments (85%) occurred in eyes with pared to SS patients (120) - whe.reas nation­ pre-existing vitreous haemorrhage. Involve­ ally the SS genotype (0.4% live births) is ment of the posterior pole usually results in more prevalent than SC genotype (0.2% live severe visual loss difficult to treat by conven­ births). Thus, although the study group is not tional surgery9 although occasionally amena­ representative of patients with sickling ble to therapy with the Neodymium:YAG haemoglobinopathies per se, the prevalence, laser. Rhegmatogenous retinal detachment incidence and causes of visual loss in PSR (Fig 3) is uncommon in sickle cell retinopathy and non-PSR groups is valid. but may result from traction on thin atrophic Visual loss in sickle cell retinopathy is prin­ retina. cipally determined by PSR which predisposes Epiretinal membranes may be responsible to vitreous haemorrhage, vitreous traction, for moderate visual loss in sickle cell disease, retinal detachment, and epiretinal membrane and occasionally a localised associated trac­ formation. 8 Auto-infarction of PSR may tional retinal detachment (Fig 4) may result reduce the chance of visual loss but the pre­ in severe visual loss. Risk factors for ERM sent study indicates that a considerable risk of visual loss remains. Vitreous haemorrhage was the most frequent cause of both 'moder­ ate' and 'severe' visual loss. Risk factors for vitreous haemorrhage have been identified as the SC genotype, pre­ sence of previous vitreous haemorrhage, and PSR involving more than 60° of the retinal circumference.6 Iron and blood products from previous haemorrhage may accelerate vitreous degeneration, causing further trac­ tion and predisposing to further more persis­ tent, vitreous haemorrhage and/or a trac­ tional detachment. Tractional retinal detachment (Fig 2) Fig. 3.
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