Case Presentation: A 73-year-old woman with type II diabetes presented with right eye pain and decreased vision. On exam, she had right eye periorbital edema, conjunctival injection, and corneal opacification. Laboratory studies revealed Streptococcus pneumoniae bloodstream infection and meningitis. Imaging demonstrated leptomeningeal enhancement, debris in the occipital horns and fourth ventricle consistent with ventriculitis, and right orbit/globe inflammatory changes consistent with panophthalmitis. Intravenous and intravitreal antibiotics were initiated. On day 3, she developed intermittent bradycardia (HR 20-30s) and sinus pauses lasting 10-20 seconds. Examination revealed severely elevated intraocular pressures (IOPs) (52mmHg, normal range: 10-21 mmHg), and she was given intravitreal dexamethasone and maximal topical pressure-lowering agents. As her intraocular pressures decreased, her sinus pauses shortened, and her bradycardia improved. On day 10, she again developed bradycardia (HR 20-30s), alternating with atrial fibrillation with rapid ventricular response (HR 150-160s). She also began experiencing severe right eye pain requiring fentanyl infusion and ultimately sedation. IOPs were again elevated (34mmHg). IOP-lowering drops were restarted, with improvement in her sinus pauses and bradycardia. The patient continued to suffer from intractable eye pain, and ultimately, the decision was made to pursue enucleation, after which she did not experience issues with bradycardia or sinus pauses for the remainder of her hospital stay.

Discussion: The oculocardiac reflex is defined by a >20% decrease in heart rate following direct globe pressure or traction on the extraocular muscles. This reflex usually causes sinus bradycardia but has been associated with several arrhythmias including sinus node dysfunction and atrial fibrillation. Classically, this reflex is considered a transient and exhaustible phenomenon most commonly encountered intraoperatively. However, there have been reports of the oculo-cardiac reflex as a more sustained phenomenon. One case reported episodic bradycardia for several years that resolved after surgical removal of an intraocular foreign body. Another reported constant bradycardia (>48 hours) after repair of a right globe perforation that did not resolve until surgical removal of an orbital foreign body. In our case, there was a clear temporal association of her bradycardia with elevated intraocular pressure, possibly due to intraocular and extraocular inflammation as well as external globe pressure from a tight, edematous eyelid. Unfortunately, we cannot offer definitive evidence of this suggested mechanism as we did not attempt to alter vagal tone. It is possible that her bradycardia and sinus pauses could be partly explained by increased vagal tone in the setting of severe eye pain. However, her rate and rhythm improved with intraocular pressure control despite inadequate pain control. We considered meningitis-induced Cushing reflex as a mechanistic explanation of her bradycardia but felt this was less likely given she remained normotensive without elevated pulse pressure.

Conclusions: We describe a patient with suspected oculocardiac reflex-mediated arrhythmia in the setting of severe right globe infection and inflammation. This case adds to a limited body of literature suggesting that oculocardiac reflex may manifest as a prolonged phenomenon, and in this setting, use of IOP-lowering agents may aid in the management of these arrythmias.

IMAGE 1: FIGURE 1: Initial external eye exam

IMAGE 2: FIGURE 2: Heart rate vs. intraocular pressure