Steroid Response Following Dropless Cataract Surgery Using Subconjunctival Triamcinolone

Abstract

Purpose

To assess the rates of postoperative steroid response following dropless cataract surgery using a subconjunctival depot of triamcinolone versus conventional cataract surgery using topical prednisolone.

Patients and Methods

We reviewed consecutive cataract surgery cases performed by a single surgeon to determine the likelihood of steroid response, defined as intraocular pressure (IOP) 50% above baseline or IOP > 24 mmHg postoperatively, excluding the first 72 hours. Logistic regression models were performed including baseline characteristics as exposures in the model and steroid response as the outcome. Main outcome measures were the proportion of eyes developing steroid response, risk factors for developing steroid response, and duration of steroid response.

Results

Of the 150 dropless and 218 conventional cases, 26 eyes developed steroid response (15 dropless and 11 conventional cases [10% vs 5%, P=0.096]). Risk factors for steroid response included dropless surgery (OR=2.43, 95% CI=1.03–6.02], P=0.046) and prior diagnosis of glaucoma (OR=7.18, 95% CI=2.66–19.22], P<0.001). Baseline IOP, age, sex, race, and axial length did not increase risk for steroid response. Of the eyes with steroid response, more dropless cases had an IOP elevation ≥30 days (9/15 eyes vs 1/11 eyes; P=0.008), including one patient with refractory IOP elevation in the dropless group who required urgent bilateral trabeculectomy for IOP control.

Conclusion

Dropless cataract surgery increases the risk of prolonged steroid response postoperatively. Patients with glaucoma have an increased risk of steroid response and may not be good candidates for dropless cataract surgery with subconjunctival triamcinolone.

Keywords:

• ocular hypertension
• glaucoma
• intraocular pressure
• triamcinolone depot
• postoperative

Acknowledgments

Lucy Q Shen and Milica A Margeta are co-senior authors for this study.

Disclosure

M. A. M. has been supported by NIH/NEI K12 EY016335, NIH/NEI K08 EY030160, an American Glaucoma Society Young Clinician Scientist Award, a Research to Prevent Blindness Career Development Award, Glaucoma Research Foundation Catalyst for a Cure Initiative to Prevent and Cure Neurodegeneration Award, Alcon Research Institute Young Investigator Award, Massachusetts Lions Eye Research Fund, Robert M. Sinskey Foundation, Ruettgers Family Charitable Foundation, and B.L. Manger Foundation. M. A. M. is also a consultant for Idorsia Pharmaceuticals. L. Q. S. is supported by NIH/NEI R01EY031696. L. Q. S. is also a consultant for FireCyte Therapeutics, Inc and AbbVie Inc. M. W. is supported by NIH R00 EY028631, Research to Prevent Blindness International Research Collaborators Award and Alcon Young Investigator Grant. R. P. is a consultant for Sanofi-Genzyme and Elsevier. The authors report no other conflicts of interest in this work.