Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

Purpose: To report a case of interface fluid syndrome following small incision lenticule extraction (SMILE) and subsequent CIRCLE enhancement. Case Presentation: A 30-year-old female experienced progressively worsening vision following refractive enhancement surgery. The patient had experienced a transient increase in intraocular pressure (IOP) after SMILE, normalized poststeroid cessation. Three months after the enhancement, her best-corrected visual acuity deteriorated from 20/20 in both eyes before the surgery to 20/300. IOP measured by non-contact tonometry was 25.3 mmHg in the right eye and 26.7 mmHg in the left eye, while the measurements off the flap using iCare were 55.3 mmHg and 47.8 mmHg, respectively. Examination revealed moderate corneal edema, interface fluid pockets, and haze, which were confirmed by anterior segment optical coherence tomography. Treatment involved the discontinuation of steroids and the introduction of hypotensive medication, leading to significant symptom relief. Conclusion: This case highlights the importance of cautious and conservative steroid use, particularly in steroid-responsive patients. When steroids are administered in cases potentially involving diffuse lamellar keratitis and haze, monitoring peripheral IOP is essential.

Purpose: To report a case of interface fluid syndrome following small incision lenticule extraction (SMILE) and subsequent CIRCLE enhancement. Case Presentation: A 30-year-old female experienced progressively worsening vision following refractive enhancement surgery. The patient had experienced a transient increase in intraocular pressure (IOP) after SMILE, normalized poststeroid cessation. Three months after the enhancement, her best-corrected visual acuity deteriorated from 20/20 in both eyes before the surgery to 20/300. IOP measured by non-contact tonometry was 25.3 mmHg in the right eye and 26.7 mmHg in the left eye, while the measurements off the flap using iCare were 55.3 mmHg and 47.8 mmHg, respectively. Examination revealed moderate corneal edema, interface fluid pockets, and haze, which were confirmed by anterior segment optical coherence tomography. Treatment involved the discontinuation of steroids and the introduction of hypotensive medication, leading to significant symptom relief. Conclusion: This case highlights the importance of cautious and conservative steroid use, particularly in steroid-responsive patients. When steroids are administered in cases potentially involving diffuse lamellar keratitis and haze, monitoring peripheral IOP is essential.