The global diabetes epidemic continues to rise, with complications extending beyond diabetic retinopathy (DR) and cataracts to include dry eye syndrome (DES), or keratoconjunctivitis sicca. Approximately 54% of individuals with diabetes experience DES, yet the condition remains poorly understood. Diabetes mellitus (DM) disrupts tear film homeostasis through mechanisms such as lacrimal gland dysfunction, Meibomian gland dysfunction, and abnormal tear dynamics. Chronic hyperglycemia, diabetic neuropathy, systemic inflammation, and altered mucin secretion exacerbate these changes, leading to tear instability and ocular surface damage. Risk factors for DES include advanced age, female sex, smoking, and higher glycated hemoglobin (HbA1c) levels. Surgical interventions for diabetes-related ocular complications, such as cataract surgery, intravitreal injections, and pan-retinal photocoagulation, further increase the risk of DES. Treatment strategies for diabetic dry eye (DMDES) include artificial tears, anti-inflammatory drugs like corticosteroids, cyclosporin A, tacrolimus, and autologous blood serum. However, these treatments address symptoms rather than underlying causes, with potential side effects. Emerging therapies, including gene-based approaches, show promise but require further research. Given the high prevalence of DMDES and its potential impact on quality of life, routine ocular surface and tear function assessments are recommended in diabetic care. Early diagnosis, glycemic control, and personalized treatment regimens are critical for preventing complications. Future studies must focus on targeted therapies to better manage DMDES and improve patient outcomes.