Effect of Nd:YAG laser posterior capsulotomy on intraocular pressure in diabetic patients

Thabet Mohammed, Shimaa Mohammed; Hassanin, Rabei Mohammed Mohammed; Khalil, Mohamed Farag; Mahmoud, Mohamed Salah El-Din

doi:10.21608/mjmr.2025.402821.2029

Effect of Nd:YAG laser posterior capsulotomy on intraocular pressure in diabetic patients

Articles in Press

Document Type : Original Article

Authors

¹ Department of ophthalmology, Faculty of medicine , Minia university, ElMinia, Eygpt

² Ophthalmology department Faculty of Medicine Minia University, Minia , Egypt

10.21608/mjmr.2025.402821.2029

Abstract

Introduction :

Months to years following cataract surgery, posterior capsule opacification (PCO) develops due to the presence of a mixture of scar-producing myofibroblasts and aberrant lens fiber cells in the optical axis [1]

Visual acuity& contrast sensitivity are impaired in considerable PCO. The first-line treatment option is posterior capsulotomy performed with Neodymium:Yttrium – Aluminum–Garnet (Nd:YAG) laser which can be simply performed in a short time as an outpatient procedure. [1]

Following Nd:YAG laser procedure some complications have been reported that can be detected by routine examination include intraocular lens injury, iritis, vitritis, cystoid macular edema (CME), and changes in refraction and intraocular pressure (IOP). [2]

The most common complication of posterior capsulotomy is increased IOP. Different explanations which have been given for the pressure rise following Nd: YAG laser treatment include the deposition of debris in the trabecular meshwork, pupillary block, and inflammatory swelling of the ciliary body or iris root associated with angle closure. Despite the prophylactic treatment, increased IOP was reported in 15% to 30% of patients in several studies [3].

Diabetic patients are at higher risk of complications after surgery and developing macular edema after YAG laser. So evaluation of macula before and after YAG laser is very important [4].

The rise in IOP after YAG has been documented in various studies up to 30% above the baseline levels , The mechanism of this increase is thought to be multifactorial , involving inflammation , the release of inflammatory mediators ,and disruption of the aqueous outflow pathways.[5]

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