Sridhar Uma, Tripathy Koushik
ICARE Eye Hospital and Post Graduate Institute
ASG Eye Hospital, BT Road, Kolkata, India
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.
“晶状体过敏性眼内炎”这一术语由韦尔霍夫和勒莫因于1922年提出，当时他们报告了一些患者，这些患者在接受囊外白内障摘除术后出现炎症加重（明显是类似眼内炎的无菌性炎症）。然而，这种疾病实体最早是由施特劳布在1919年认识到的。当大多数患者对皮内注射晶状体蛋白产生反应时，这种病症的免疫性质得到了证实。这种晶状体诱导的炎症（葡萄膜炎）的其他名称包括晶状体溶解性青光眼、晶状体源性葡萄膜炎、晶状体毒性葡萄膜炎和晶状体过敏性眼内炎。晶状体诱导的炎症有免疫基础，但不涉及免疫球蛋白E或组胺（如I型超敏反应所见）。因此，现在不提倡使用“晶状体过敏性眼内炎”这一术语。“晶状体毒性葡萄膜炎”这一术语也应避免使用，因为尚未证明晶状体蛋白对眼睛有毒性。晶状体蛋白暴露于免疫系统或对晶状体蛋白的免疫耐受性改变被认为会导致晶状体诱导的炎症。晶状体诱导的炎症发生在各种临床情况下，包括晚期白内障中晶状体蛋白通过完整的晶状体囊渗漏（晶状体溶解性葡萄膜炎或晶状体溶解性青光眼）以及外伤性白内障或白内障手术后前晶状体囊破裂（晶状体抗原性葡萄膜炎）。在现代白内障手术中，白内障手术后残留皮质并不常见。然而，当白内障摘除术后有残留皮质时，无论后囊是否完整，都可能发生炎症。这种炎症可能表现为眼部发红、疼痛和畏光。通常，晶状体诱导的炎症在白内障手术或清除残留晶状体物质后得到控制。本综述讨论了晶状体诱导炎症的病因、病理生理学、临床体征和症状、鉴别诊断以及治疗。
