To investigate the effect of serial anterior chamber (AC) paracenteses in eyes with sustained elevations of intraocular pressure (IOP) in the setting of repeated intravitreal injections (IVI) of anti–vascular endothelial growth factor medications.
This is a retrospective records review of patients undergoing IVI of anti–vascular endothelial growth factor medication (bevacizumab, ranubizumab, or aflibercept), who demonstrated a sustained elevation of preinjection IOP and also received AC paracentesis immediately after IVI on at least three consecutive visits. Changes in preinjection IOP and cup-to-disk (C:D) ratio were compared before and after the initiation of IVI and before and after the introduction of AC paracenteses with each subsequent IVI.
Twenty-three eyes of 17 patients receiving a median of 26 IVI experienced a rise in preinjection IOP from 16.3 mmHg to 21.1 mmHg (P = 0.004) and an increase in mean C:D ratio from 0.37 to 0.47 (P = 0.0002). After introduction of AC paracenteses (median of 12), mean IOP was returned to baseline 16.00 mmHg (P = 0.002), mean C:D ratio stabilized (0.50, P = 0.197), and maximum IOP decreased from 26.8 mmHg to 23.0 mmHg (P = 0.05). Nineteen (82.6%) eyes required an increase in topical glaucoma medications during the study period, and 13 (56.5%) still required additional therapies after initiation of AC paracenteses. Five eyes (38.5%) required laser or glaucoma drainage device procedures.
Serial AC paracenteses reduced immediate postinjection IOP, and along with standard glaucoma care in most patients, reversed preinjection IOP elevation, and stabilized optic nerve changes associated with repeated intravitreal anti–vascular endothelial growth factor injections in a subset of patients with sustained elevation of preinjection IOP.
Sustained intraocular pressure elevation occurs in a minority of patients receiving intravitreal anti–vascular endothelial growth factor injections. Treatment with anterior chamber paracentesis along with standard of care management of ocular hypertension, returned preinjection intraocular pressure to baseline and halted further glaucomatous disk damage.
*Department of Ophthalmology, University of Cincinnati, Cincinnati, Ohio; and
†Cincinnati Eye Institute, Cincinnati, Ohio.
Reprint requests: Robert A. Sisk, MD, Cincinnati Eye Institute, 1945 CEI Drive, Cincinnati, OH 45242; e-mail: email@example.com
None of the authors has any financial/conflicting interests to disclose.