Safety of intracameral phenylephrine

I read with interest the article by Shams et al.1 on systemic complications of phenylephrine used in the preoperative period and agree with their recommendation that patients receiving topical phenylephrine might benefit from cardiac and blood pressure monitoring. It is unclear from their article whether topical preoperative phenylephrine drops were also used. The peak plasma level of phenylephrine after preoperative drops is 15 to 20 minutes,2 which reflects the time course in their patient. Plasma levels after intracameral phenylephrine, unlike with topical administration, have not been measured and must be lower due to the blood–eye barrier and lesser dose. When one reviews the physiologic cardiac responses to phenylephrine, ventricular fibrillation is unlikely to be related to phenylephrine, whether applied topically or intracamerally. Ear, nose, and throat use of large doses of phenylephrine has been reported to cause severe cardiovascular compromise and possibly death.3 Although phenylephrine is predominantly a selective α-agonist, at very high doses β activation does occur. Patients might demonstrate a marked bradycardia in response to hypertension, suggesting mainly an α-1–mediated vasoconstriction and a baroreceptor-mediated bradycardia. Phenylephrine also increases the energy required to induce ventricular fibrillation in humans. Phenylephrine infusion has differential electrophysiologic effects in atrial and ventricular tissue. Rather than being proarrhythmic, phenylephrine might be protective against arrhythmias because it effectively terminates supraventricular tachycardias and might be protective against ventricular arrhythmias.4 Of greater concern is the anesthesiologist’s response to phenylephrine-induced hypertension, especially with bradycardia. Labetalol is readily available and is a drug most anesthesiologists have experience using for intraoperative hypertension. It is a mixed α-antagonist and β-antagonist, although the β effects are about 7 times stronger than the α effects. Beta antagonists might result in the inability of the heart to compensate for the increased after-load, leading to pulmonary edema.5 A New York State report on phenylephrine use in the operating room6 recommended that severe hypertension or associated complications (pulmonary edema or electrocardiogram changes) should be treated with direct vasodilators or α-antagonists, such as phentolamine, rather than β-blockers. I routinely use a compounded solution of phenylephrine 1.5% and lidocaine 1.0% solution as the sole method of pupil dilation as well as for prophylaxis against intraoperative floppy-iris syndrome. I have never had patients with monitored anesthesia care develop new ventricular arrhythmias, while only occasionally do some need management for hypertension. The dose from an intracameral placement of 0.2 mL of phenylephrine 1.5% is exceedingly low, making the risk for systemic complications even lower than that of topical phenylephrine 2.5% drops, a practice deemed safe based on a recent review and metaanalysis.7