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Kerato‐conjunctivitis sicca and cataracts are the two most common late complications affecting the anterior segment of the eye.

Cataract formation, particularly posterior sub‐capsular cataracts, has long been recognized in recipients of hematopoietic HSCT [19, 20]. The two main risk factors for cataract development are exposure to TBI and steroids therapy for cGVHD [19–21]. After single‐dose TBI, almost all patients developed cataracts within 3 to 4 years, and most, if not all, need surgical repair. The probability of developing cataracts after fractionated TBI is in the range of 30% at 3 years, but may be as high as 80% at 6 to 10 years after HSCT. In a multivariate analysis, the use of TBI, single as compared to fractionated dose TBI, and the use of steroid treatment for longer than 3 months were associated with a significantly increased risk of cataract development [21]. The radiation effect was dose‐rate dependent [22,23]. The largest series to date included a cohort of 1064 patients and identified as factors independently associated with an increased risk of cataracts; older age (>23 years), higher radiation exposure rate (>4 cGy/min), allogeneic rather than autologous HSCT, and steroid administration [22,23]. Finally, in prospective studies comparing the incidence of cataracts and predisposing risk factors, patients who received cyclophosphamide and TBI (Cy/TBI) had a higher incidence of cataracts than patients treated with busulfan and Cy (Bu/Cy) [24].

Kerato‐conjunctivitis sicca of the eyes is usually part of a more general syndrome that also includes xerostomia, dryness of the skin, and, in women, vaginitis. All these manifestations are closely related to cGVHD [25–28]. In its most extensive form, the clinical picture may be that of a Sjögren‐like syndrome, as described in detail in other chapters of this book.