Lens-Induced Inflammation

The term 'endophthalmitis phacoanaphylatica' was introduced by Verhoeff and Lemoine in 1922 when they reported patients who had increased inflammation (apparently sterile inflammation mimicking endophthalmitis) after they underwent extracapsular cataract surgery. This disease entity was, however, recognized first by Straub in 1919. The immunological nature of this condition was proved when most patients reacted to an intracutaneous injection of lens proteins. Other names of such lens-induced inflammation (uveitis) include phacolytic glaucoma, phacogenic uveitis, phacotoxic uveitis, and phacoanaphylactic endophthalmitis. Lens-induced inflammation has an immune basis, but it does not involve immunoglobulin E or histamine (as seen in type I hypersensitivity reaction). Thus the term phacoanaphylactic endophthalmitis is not preferred now.  The term phacotoxic uveitis is also avoided as lens protein has not proven toxic to the eye. Exposure of the lens proteins to the immune system or alteration of immune tolerance to lens protein is supposed to cause lens-induced inflammation. Lens-induced inflammation occurs in various clinical scenarios, including leakage of lens proteins through an intact lens capsule in advanced cataracts (phacolytic uveitis or phacolytic glaucoma) and a broken anterior lens capsule in traumatic cataracts or after cataract surgery (phacoantigenic uveitis).  In modern-day cataract surgery, the retained cortical matter is not very commonly seen after cataract surgery. However, when there is residual cortex after cataract removal, with or without an intact posterior capsule, inflammation can occur. Such inflammation may present with ocular redness, pain, and sensitivity to light. Typically, lens-induced inflammation gets controlled after cataract surgery or removal of the retained lens matter. This review discusses the etiology, pathophysiology, clinical signs and symptoms, differential diagnoses, and the management of lens-induced inflammations.