A 42-year-old Indian man on long-term oral corticosteroids for systemic lupus erythematosus presents with complaints of difficulty reading and glare in bright sunlight for the past 6 months. On slit-lamp examination, a plaque-like opacity is seen at the posterior pole of the lens, just anterior to the capsule. Visual acuity is 6/18. What is the most likely diagnosis?

Explanation

## Diagnosis: Posterior Subcapsular Cataract (PSC) ### Clinical Presentation The patient presents with: - **Steroid use** (long-term oral corticosteroids for SLE) - **Rapid onset** over 6 months (much faster than age-related cataracts) - **Glare and dysphotopsia** (hallmark symptom) - **Difficulty reading** (near vision affected disproportionately) - **Plaque-like opacity at posterior pole**, just anterior to the capsule ### Key Features of Posterior Subcapsular Cataract **Key Point:** Posterior subcapsular cataracts are the most common **steroid-induced cataract** and can develop rapidly, even within months of initiating corticosteroid therapy. **High-Yield:** PSC is the only cataract type where **glare and dysphotopsia are the predominant symptoms**—patients often complain of difficulty with bright light and reading despite relatively preserved distance vision. ### Comparison of Cataract Types | Feature | Posterior Subcapsular | Nuclear Sclerotic | Cortical | |---------|----------------------|-------------------|----------| | **Risk factors** | Steroids, trauma, uveitis, radiation | Age | Age, metabolic disease | | **Onset** | Rapid (months) | Insidious (years) | Variable | | **Primary symptom** | Glare, dysphotopsia, reading difficulty | Myopic shift, presbyopia | Glare, blurred vision | | **Location** | Posterior pole (subcapsular) | Nucleus | Cortex (radial spokes) | | **Appearance** | Plaque-like, bread-crumb pattern | Brown/amber nucleus | Vacuoles, radial opacities | | **VA vs. symptoms** | Disproportionate glare (VA better than symptoms) | Proportionate vision loss | Proportionate vision loss | ### Pathophysiology of Steroid-Induced PSC **Mnemonic: STEROIDS cause PSC via:** - **S**orbitol accumulation (osmotic stress) - **T**ransport disruption (Na⁺/K⁺-ATPase inhibition) - **E**nzyme inhibition (aldose reductase pathway) - **R**eactive oxygen species (oxidative stress) - **O**smotic imbalance (water influx) - **I**nflammation and protein denaturation - **D**amage to posterior epithelial cells - **S**ubcapsular lens fiber swelling and opacity **Clinical Pearl:** The posterior location of PSC explains why glare is so prominent—light rays passing through the posterior opacity are scattered directly onto the macula, causing disproportionate symptoms relative to visual acuity. ### Why Posterior Subcapsular Cataract? The **rapid 6-month onset** in a steroid-treated patient with **plaque-like posterior pole opacity** and **glare as the dominant symptom** is pathognomonic for steroid-induced posterior subcapsular cataract. This is a well-recognized iatrogenic complication of prolonged corticosteroid therapy.