Acute painful visual loss from accelerated hypertensive choroidopathy

Abstract

32-year-old man presented witha 2-day history of redness,severe pain and reduced vision in theright eye. Best corrected visual acuity(VA) was 6⁄9 and 6⁄6 in the right andleft eyes, respectively. He had no pastmedical or ophthalmic history. Slit-lamp examination showed right con-junctiva injection and the anteriorchamber (AC) was considerably shal-low with no cornea and pupil abnor-malities. His left eye was normal.Intraocular pressure (IOP) was20 mmHg in both eyes. Gonioscopyrevealed the iridocorneal angle in theright eye to be closed, whereas that inthe left eye was wide open. Fundusexamination confirmed hypertensiveretinopathy in both eyes (Fig. 1A, B),with haemorrhagic ciliochoroidaldetachment in the right eye (Fig. 1C).The subject’s blood pressure raisedto 220⁄150 mmHg. An ultrasoundB-scan of the right eye (Fig. 1D)showed diffuse shallow haemorrhagicchoroidal detachment in the temporalquadrant. Neodymium yttrium alu-minium garnet (Nd:YAG) laser per-ipheral iridotomy failed to deepen theright AC. The subject was managedmedically with topical intensive ster-oid and oral analgesics. Acetazola-mide 250 mg three times daily wasadded for 1 day to prevent a postNd:YAG IOP spike. He was referredurgently to a physician for control ofsystemic hypertension. One monthlater, best corrected VA in the righteye was 6⁄6 and the AC was deep.The haemorrhagic ciliochoroidaldetachment had resolved with mini-mum retinal pigment epithelium(RPE) changes at the macula.Spontaneous choroidal detachmentcausing secondary angle-closure glau-coma has numerous associations, suchas uveal effusion syndrome, scleritis,carotid cavernous fistulas, Harada’sdisease and acquired immunodefi-ciency syndrome (Pesin et al. 1990).Renal hypertension presenting asacute angle-closure glaucoma secon-dary to serous retinal detachment ingrade IV hypertensive retinopathy hasbeen reported previously (Arora et al.1991; Pierro et al. 1991).Acute angle closure due to haemor-rhagic ciliochoroidal detachment as acomplication of hypertensive choroid-opathy is unusual (Pesin et al. 1990).It induced transient myopia andintractable ocular pain in our patient,who had previously undetected accel-erated hypertension. The mechanismof angle closure involved forward bul-ging of the iris lens diaphragm follow-ing haemorrhagic ciliochoroidaldetachment. The painful visual loss isattributed to ciliochoroidal ischaemiaand haemorrhagic infarction (Kiny-oun & Kalina 1986). The symptomswere highly suggestive of anteriorischaemic ocular syndrome or ‘ocularangina’. The underlying causes of thechoroidal haemorrhage were suddenincreasing blood pressure, increasingsympathetic tone, fragility of choroi-dal vessels and haemorrhagic choroi-dal infarction.Accelerated essential hypertensionwas the only associated condition inthis patient after endocrine, renal andcollagen vascular diseases had beenexcluded. He had been unaware of hishypertension until he presented withacute visual loss. Nd:YAG peripheraliridotomy was attempted to preventperipheral anterior synechiae and sec-ondary glaucoma, but was ineffective.With hindsight, achieving control ofblood pressure prior to undergoingYAG peripheral iridotomy might havebeen preferable as the subject’s IOPwas normal at presentation.Hypertensive choroidopathy is asimportant a fundus change as hyper-tensive retinopathy (Hayreh et al.1986). In hypertensive choroidopathy,the choroidal vascular bed showsextensive occlusion and ischaemicchanges (Hayreh et al. 1986). LateRPE changes in the macula are asequaela to RPE infarction associatedwith occlusion of choroidal capillaries.Massive spontaneous choroidal hae-