Oculocardiac reflex: An infrequent occurrence noted during pupillometry assessments

Dear Sir,

The oculocardiac reflex (OCR) is mediated through the trigeminal-vagal pathway. It manifests as bradycardia and hypotension due to pressure on the extraocular muscles.^[1] A 35-year-old male patient arrived with a history of a road traffic accident. In the emergency department, he exhibited a Glasgow Coma Scale score of E2V2M2.

He was intubated and shifted for imaging. A computed tomography scan of the brain showed bilateral frontal hemorrhagic contusions, traumatic subarachnoid hemorrhage, pneumocephalus, tentorial subdural hemorrhage, and brain stem hemorrhage. The patient also had comminuted fractures in the roof, medial wall, and floor of both orbits, with air foci and bony fragments present in the cavity. He was shifted to the intensive care unit for further management [Figure 1].

Close

Figure 1:

(a) Axial section of CT with orbital fracture (white arrow) (b) Impacted foreign body in the orbit with multiple air foci (red arrow).

Export to PPT

After initial stabilization, as part of the neurological examination, we performed pupillometry. During this noninvasive procedure, in which the eye cup was gently placed on the orbital rim [Figure 2], we observed a sudden change in the heart rate from 113 beats/min to 87 beats/min, associated with hypotension (87/44 mmHg). Due to the hypotension, injection of ephedrine 6 mg stat, was given immediately. The reflex was spontaneously abolished once the pupillometer was removed from the orbital rim. The examination of the eyes, including visual pursuit and visual acuity, could not be performed because he was deeply sedated.

Close

Figure 2:

Pupillometry examination of the eye.

Export to PPT

OCR is a physiological phenomenon described by Aschner B.^[2] OCR is characterized by bradycardia due to intraocular tension and traction on the extraocular muscles, particularly the medial rectus muscle.^[3] Compression on the globe stimulates the stretch receptors on the afferent limb of the ciliary ganglion, and the ophthalmic division of the trigeminal nerve terminates in the sensory nucleus of the trigeminal nerve. The efferent impulse is mediated through the motor nucleus of the vagus nerve, leading to bradycardia and reduced cardiac output.

It is frequently observed during strabismus surgery and other ocular procedures following orbital trauma. However, OCR’s association with orbital fractures in the critical care setting is rare compared to its occurrence during operative procedures.

Bradycardia may resolve on its own after the stimulus is removed, but it can be severe enough to cause hemodynamic fluctuations, ventricular arrhythmias, and, in extreme cases, asystole.

The risk of fatal arrhythmia due to OCR is about 1:3500. Rarely, OCR has also been associated with death.^[4] It can be pharmacologically treated with injection of atropine 0.02 mg/kg through the intravenous route or injection of glycopyrrolate 0.01 mg/kg.^[5]

Hypotension in severe trauma can result from hemorrhagic, neurogenic, and cardiogenic causes. Bradycardia may occur in the context of hypoxia, hypothermia, and the use of inotropic agents. OCR led to a temporary drop in blood pressure along with an increase in inotropic support. These hemodynamic fluctuations contribute to poor neurological outcomes. In our situation, OCR likely occurred due to an impacted foreign body combined with compression on the globe by the pupillometer eye cup.

However, OCR has not yet been described during pupillometry examinations. Although it is a noninvasive method, even gentle pressure on the orbit triggers this reflex. This is the first report of OCR during pupillometry. In instances of acute brain injury, it is essential to exercise caution at every stage of patient care, even when conducting non-invasive procedures and maneuvres.