A comprehensive review on Chandler’s syndrome: Pathophysiology, diagnosis, management, and future perspectives

Chandler's Syndrome, a rare variant of iridocorneal endothelial (ICE) syndrome, is characterized by corneal endothelial abnormalities, iris atrophy, and secondary glaucoma. This review highlights this progressive condition's clinical presentation, pathophysiology, diagnosis, and management. Chandler's Syndrome primarily affects middle-aged Caucasian women and presents with unilateral corneal edema, visual disturbances, and subtle iris changes. Endothelial cell proliferation and migration lead to peripheral anterior synechiae (PAS), elevated intraocular pressure (IOP), and corneal decompensation. While the exact etiology remains unclear, viral infections such as herpes simplex (HSV) and Epstein-Barr (EBV) are hypothesized contributors. Morphological changes, including metaplasia of endothelial cells and ectopic membrane formation, further compromise aqueous outflow and corneal integrity. Diagnosis relies on slit-lamp examination, specular and confocal microscopy, and ultrasound biomicroscopy (UBM) to detect endothelial abnormalities and anterior segment changes. Differential diagnosis with conditions like posterior polymorphous corneal dystrophy (PPCD) and Fuchs' dystrophy is critical for accurate assessment. Management includes medical therapy to control IOP and surgical interventions like trabeculectomy, glaucoma drainage implants, and corneal procedures such as Descemet stripping endothelial keratoplasty (DSEK) or penetrating keratoplasty (PK). Long-term follow-up is essential to monitor disease progression and preserve visual function. Future research into the viral pathogenesis and mechanisms of endothelial dysfunction is vital to advance targeted therapies.