Simultaneous bilateral visual loss caused by rupture of retinal arterial macroaneurysms in a hypertensive patient

Authors


Panagiotis G. Theodossiadis MD
13 Lykiou Street
106 74 Athens
Greece
Tel: + 30 210 72 57 585
Fax: + 30 210 72 95 318
Email: george@hellasnet.gr

Sir,

Retinal arterial macroaneurysms develop in the course of hypertensive vascular disease, affecting usually elderly patients (Panton et al. 1990). They occur in the first three bifurcations of the central retinal artery. Histopathologically, macroaneurysms are caused by a break in the internal elastic lamina of the artery wall, through which blood components such as serum, lipid exudates and blood itself find access and leak into the surrounding retina. Deposition of these substances in the macular area may result in visual loss (Gass 1997; Spaide 1999). Retinal arterial macroaneurysms are usually unilateral. In 10% of patients with hypertensive, uncontrolled vascular disease they may occur bilaterally (Kayazawa 1980).

We present a 77-year-old woman with severe hypertension and sudden, simultaneous, bilateral visual loss, who was first examined in September 2002. She complained of bilateral, simultaneous, acute loss of central vision, which had occurred after strenuous physical effort 20 days earlier. The medical history was remarkable for hypertension. On ophthalmic examination, her visual acuity (VA) was hand motion in the right eye and counting fingers in the left eye. Pupillary reactions were normal. Slit-lamp examination of the anterior segment was unremarkable in both eyes. Dilated fundoscopy showed bilateral subinternal limiting membrane haemorrhages covering both posterior poles (Figs. 1 and 2). The haemorrhage in the right eye had an orange-coloured appearance, and contained lipid exudates and serum (Fig. 1). Fluorescein angiography in each eye at presentation showed an area of hypofluorescence caused by the haemorrhage and a round area of hyperfluorescence corresponding to the retinal macroaneurysms (Figs. 1 and 2). Indocyanine green angiography (ICG) demonstrated a well defined area of hyperfluorescence, which corresponded to the macroaneurysms, which were located in the superotemporal arterial arcade in the right eye and in a branch of the inferotemporal arcade in the left eye (Figs. 1 and 2). The patient's blood pressure was 190/120 mmHg.

Figure 1.

(A) Right eye: haemorrhage in the macula containing lipid exudates and serum. The macroaneurysm in the superotemporal arcade is ill defined. (B) Fluorescein angiogram demonstrates the typical round dilatation adjacent to the upper temporal branch of the central artery. (C) The ruptured retinal macroaneurysm located in the superotemporal arcade becomes more evident by ICG.

Figure 2.

(A) Left eye: haemorrhage in the macula. (B) Fluorescein angiogram shows the hyperfluorescent retinal macroaneurysm located in a branch of the inferotemporal arterial arcade. (C) The ruptured retinal macroaneurysm is more evident by ICG.

Magnetic resonance imaging of the brain revealed chronic focal ischaemic changes, which were consistent with her uncontrolled high blood pressure (Fig. 3).

Figure 3.

Brain magnetic resonance T2 weighted image showing chronic focal ischaemic changes due to atherosclerotic vascular disease.

The haemorrhages in both eyes did not resolve and, therefore, 50 days after the first examination, laser photocoagulation was performed. Six months after the laser application, the haemorrhages had absorbed bilaterally. Best corrected VA was 20/60 in the left eye and 20/70 in the right eye.

Subretinal, intraretinal and vitreous haemorrhages are well known complications of macroaneurysms. However, simultaneous bilateral visual loss due to the rupture of macroaneurysms has not been previously reported. Conditions that can cause subretinal, intraretinal and preretinal haemorrhage apart from macroaneurysms are mainly exudative age-related macular degeneration (choroidal neovascularization; CNV) and idiopathic polypoidal choroidal vasculopathy. In such cases, where there is blood obscuring the underlying pathology, ICG angiography can help in the diagnosis. Indocyanine green angiography, in our case, did not show the characteristic polypoidal network of the choroidal vessels or the typical picture of CNV. The fact that the hyperfluorescent spot was located along the course of the retinal arterioles in both eyes confirmed our impression that it was a case of ruptured macroaneurysm. The retinal bleeding in our patient was probably caused by Valsava manoeuvre as strenuous effort had preceded the visual deterioration. The patient underwent laser treatment. Laser coagulation is indicated when the haemorrhage persists and spontaneous sealing of the arterial wall of the macroaneurysm does not occur (Bloom & Brucker 1977; Psinakis et al. 1989).

In conclusion, we present a hypertensive patient who suffered simultaneous, bilateral, central visual loss caused by the rupture of retinal arterial macroaneurysms after strenuous physical effort. It would be helpful to both physicians and ophthalmologists who treat hypertensive patients to bear in mind that rupture of pre-existing retinal arterial macroaneurysms in both eyes should be considered a possible cause of sudden, simultaneous, bilateral visual deterioration or loss.

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