Although rare, choroidal angiomas generate a disproportionate amount of interest within the profession as they cause visual loss, frequently severe, in otherwise healthy people. They are more readily diagnosed than 20 years ago as a result of modern ultrasonography and fluorescein angiography. These benign, sight threatening tumours cause visual loss by leakage of subretinal fluid.1 Symptomatic presentation occurs earlier when the haemangioma is located close to the posterior pole and within the macular arcades. Diffuse haemangiomas are usually associated with involvement of other ocular structures and with the encephalofacial angiomas as part of the Sturge–Weber syndrome; these may even be bilateral. They are congenital abnormalities, but leakage may not occur until late in the first or second decade. All ocular haemangiomas may remain occult and asymptomatic for long periods and circumscribed angiomas (which are only rarely associated with systemic abnormalities) often only present in the fourth to fifth decades. Leakage may be intermittent at first, but is later sustained.

In diffuse haemangioma of the Sturge–Weber type, ultrasound reveals that the whole choroid is slightly thickened. Leakage seems associated with the development of a localised, circumscribed choroidal nodule. Circumscribed angiomas are always unilateral and the involved area of choroid is, as the name implies, confined. There is a third group of patients who have no apparent encephalofacial involvement and who present relatively early in the second to third decades with apparently circumscribed haemangioma and yet, on ultrasound, …