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The oculocardiac reflex is a triad of bradycardia, nausea, and syncope. The ocular causes are numerous.1 Orbital causes also exist.2-4 The ophthalmic division of the trigeminal nerve is the afferent limb. The impulses pass through the reticular formation to the vagus nerve's visceral motor nuclei. The efferent limb message is carried by the vagus nerve to the heart and stomach.
We report 3 cases of orbital floor fractures that entrapped the inferior rectus muscle and/or the orbital connective tissue to immediately produce the oculocardiac reflex in 1 case and was highly suggestive in 2 others. To our knowledge, there have been no previous reports of oculocardiac reflex caused by incarceration of orbital soft tissue in an orbital trapdoor fracture.
Report of Cases
An 8-year-old boy who was pushed and hit the right side of his face, immediately developed diplopia, nausea, and vomiting. In the emergency department, his pulse rate was 58/min with a blood pressure of 111/56 mm Hg. The results of ocular examination were normal except for periorbital ecchymosis and limited vertical gaze that was worse with depression. Motility measurements revealed a 3–prism diopter (PD) right hypertropia (Figure 1, top). The computed tomographic scan revealed a nondisplaced right orbital floor fracture with incarcerated orbital soft tissue in the maxillary sinus and entrapment of the inferior rectus muscle.
Patient 1. Top, Preoperatively, the patient could not depress the right eye completely. Results of forced duction tests revealed a restrictive cause. Bottom, Postoperatively the patient was able to fully depress the right eye and denied diplopia.
The patient was taken to the operating room 2 days later where an abnormal forced duction was confirmed. During surgery the orbital connective tissue septae and fat were freed from the fracture. The inferior rectus muscle was not directly visualized. The fracture site was repaired with a shave of cranial bone. The forced duction test was repeated at the completion of the surgery and results were normal.
Postoperatively, his pulse rate was 86/min with a blood pressure of 121/63 mm Hg. The nausea and vomiting subsided. Initially there was mild limitation with depression. Thirteen months after surgery the patient was orthophoric (Figure 1, bottom).
A 12-year-old boy was hit with a brick in the right periorbital region,which causied binocular vertical diplopia, nausea, and vomiting. In the emergency department his pulse rate was 36/min with a blood pressure of 115/70 mm Hg. Results from an electrocardiogram revealed bradycardia along with some QRS complexes missing P waves. The ocular examination findings were normal except for ecchymosis on the right cheek, a 9-PD right hypotropia with limitation in upgaze, and abnormal vertical forced duction test results. The maxillary nerve sensation was symmetrically intact. The computed tomographic scan revealed a nondisplaced right orbital floor fracture with the right inferior rectus muscle entrapped in the maxillary sinus (Figure 2).
Coronal computed tomographic scan for patient 2 showing a nondisplaced orbital floor fracture with incarceration of the inferior rectus muscle in the maxillary sinus. No air-fluid level or submucosal hemorrhage is present.
The patient was taken to the operating room 7 hours later. Intravenous atropine sulfate was given prior to induction. His pulse rate ranged from 70 to 110/min. A portion of the orbital floor was removed to allow extrication of the inferior rectus muscle. The inferior rectus muscle appeared ischemic, but after delivery from the maxillary sinus, it became perfused. The floor defect was repaired with a porous polyethylene sheet. Findings from repeated forced duction tests revealed no restriction.
Postoperatively, his pulse rate remained at 60 to 70/min and all QRS complexes were associated with P waves. The nausea and vomiting subsided. The extraocular motility examination findings revealed moderate inability to depress the right globe. He was discharged and the diplopia resolved.
A 20-year-old man walked into a metal pipe striking his left cheek, which caused immediate pain, nausea, and vertical binocular double vision. His ocular examination findings were normal except for limitation of both upgaze and downgaze in the left eye. In primary gaze, he demonstrated a 6-PD left hypotropia. The computed tomographic scan revealed a nondisplaced left orbital floor fracture with soft tissue herniation into the maxillary sinus that caused entrapment of the inferior rectus muscle.
Three days later, the patient was taken to the operating room. His preoperative pulse rate was 58/min; and his blood pressure, 132/72 mm Hg. An abnormal forced duction was noted on testing. Entrapped fatty connective tissue as well as muscular tissue were released from the fracture line. The muscle contained a hematoma with signs of ischemic necrosis. The fracture was repaired with a Silastic sheet. Forced duction test results were normal. His postoperative pulse rate was 76/min with a blood pressure of 144/93 mm Hg. The nausea resolved.
Seven months after surgery, diplopia of more than 20° from primary persisted in extreme upgaze and downgaze.
The association of an oculocardiac reflex with an orbital fracture is rare, but prompt identification and treatment are important. The risk of a fatal cardiac arrhythmia exists (1:3500) with the oculocardiac reflex.5 In addition, the release of the extraocular muscle is critical for functional outcome. Hypoxia of the muscle was noted in patient 2 when intervention was undertaken 7 hours from time of the injury. Ischemic necrosis of the muscle was seen in patient 3 with a 72-hour delay prior to repair. Patient 2 had no diplopia 6 weeks after surgery while patient 3 continued to have diplopia in extreme upgaze and downgaze 7 months later. This suggests that immediate repair leads to a better motility prognosis.
Orbital trapdoor fractures are rare, occurring in children and young adults. This may be because of elasticity of the orbital bone in this age group, which allows the bone to snap into position after the soft tissue has prolapsed through the fracture. Typically, they are seen as small, nondisplaced fractures, with incarceration of the orbital connective tissue, septae, and/or the inferior rectus muscle in the maxillary sinus. This leads to restriction of motility, and the stimulation of the ophthalmic division of the trigeminal nerve triggers the oculocardiac reflex.
A patient experiencing the triad of bradycardia, nausea, and syncope following orbital injury should immediately undergo computed tomography with coronal sections. If a trapdoor fracture with incarceration of soft tissue is identified, the fracture should be repaired the same day. Timely fracture reduction and release of the muscle and/or connective tissue protect against not only life-threatening cardiac arrhythmias but also ischemic necrosis of the muscle that may lead to fibrosis and permanent restrictive strabismus.
Supported in part by a departmental award from Research to Prevent Blindness, Inc, New York, NY.
Reprints: Bryan S. Sires, MD, PhD, Harborview Medical Center, Ophthalmology, Box 359894, Seattle, WA 98104-9894 (e-mail: firstname.lastname@example.org).
Sires BS, Stanley RB, Levine LM. Oculocardiac Reflex Caused by Orbital Floor Trapdoor Fracture: An Indication for Urgent Repair. Arch Ophthalmol. 1998;116(7):955–956. doi:
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