Pupillary effects of high-dose opioid quantified with infrared pupillometry.

Abstract

The pupillary light reflex is a critical component of the neurologic examination, yet whether it is present, depressed, or absent is unknown in patients with significant opioid toxicity. Although opioids produce miosis by activating the pupillary sphincter muscle, these agents may induce significant hypercarbia and hypoxia, causing pupillary constriction to be overcome via sympathetic activation. The presence of either "pinpoint pupils" or sympathetically mediated pupillary dilation might prevent light reflex assessment. This study was designed to determine whether the light reflex remains quantifiable during opioid-induced hypercarbia and hypoxia. Ten volunteers were administered remifentanil with a gradually increasing infusion rate and intermittent boluses, until the increasing respiratory depression produced an oxyhemoglobin saturation of 85% or less with associated hypercarbia. Subjects' heart rate, blood pressure, respiration, and transcutaneous carbon dioxide level were continuously recorded. Arterial blood gases and pupillary measures were taken before opioid administration, at maximal desaturation, and 15 min after recovery. The opioid-induced oxygen desaturation (≤ 85%) was associated with significant hypercarbia and evidence of sympathetic activation. During maximal hypoxia and hypercarbia, the pupil displayed parasympathetic dominance (2.5 ± 0.2 mm diameter) with a robust quantifiable light reflex. The reflex amplitude was linearly related to pupil diameter. Opioid administration with significant accompanying hypercarbia and hypoxia results in pupil diameters of 2 to 3 mm and a reduced but quantifiable pupillary light reflex. The authors conclude that the pupillary examination and evaluation of the light reflex remain useful for neurologic assessment during opioid toxicity.