An Evidence-Based Approach to Phacomorphic Glaucoma

Cataract maturation is associated with anteroposterior lens diameter increase which, in some patients, particularly those with anatomically narrow anterior chambers, can lead to pupillary block and peripheral iridotrabecular apposition [1,2]. In other patients with previously deep anterior chambers and wide open angles, the cataract may become so swollen that it physically pushes the iris anteriorly, leading to iridotrabecular apposition [3]. The role of pupillary block in the pathophysiology of phacomorphic angle-closure is still uncertain. Limited evidence suggests that early in the course of the disease, the lens swelling is only large enough to cause pupillary block [4]. Progressive enlargement of the lens may then lead directly to peripheral iridotrabecular apposition. When the iridotrabecular apposition raises the intraocular pressure (IOP) enough to cause the signs and symptoms of an acute attack of secondary angle-closure glaucoma, it is called acute phacomorphic angle-closure. Historically this entity has been labeled phacomorphic glaucoma. As pointed out by Tham, however, using the word glaucoma implies an optic neuropathy [5]. Since many patients (as will be analyzed below) do not show glaucomatous optic neuropathy following the resolution of the acute angle-closure, it may be more accurate to call this disease acute phacomorphic angle-closure. The dense white cataract labeled as a mature cataract is an advanced form of cortical cataract, with widely hydrated cortex [6]. If the lens continues to mature and the lens protein begins to denature, the resulting hyperosmolarity leads to continued hydration and the lens becomes a swollen or intumescent cataract [7]. The lens capsule is stretched by the enlarging lens, becoming calcified in some areas and flaccid in others. Another etiology of lens hydration is traumatic puncture of the lens capsule, which follows a much more rapid course. Phacomorphic angle-closure is an uncommon condition in Western countries, though it has been cited as the cause of 3.9% of cataract extractions done in India [8]. Prevalence and incidence data is sparse. One report from Nepal Eye Hospital detailed a 2 year prevalence of 0.01% [9]. It is almost always unilateral, although one report found bilateral (but asynchronous) presentation in 14% of 86 cases [8].