Contents
Trigemino-vagal reflex associated with reduction in heart rate (> 20%) secondary to direct pressure placed on the eyeball.
Aetiology
Risk factors:
Manipulation of the extraocular muscle (EOM) through the ophthalmic branch of trigeminal nerve, stimulates the vagal center.
- Strabismus/squint surgery (traction to the extraocular muscle (EOM)) (M/C cause)
- Direct pressure to the globe
- Ocular manipulation
- Ocular pain
Clinical features
- Sinus bradycardia (M/C feature)
- Further decline to potentially fatal arrhythmias, asystole, and even cardiac arrest
Other vagal effects:
Due to the activation of the vagal motor response
- Hypotensive episodes: Syncope
- Gastrointestinal responses: Nausea and vomiting
Management
Definitive treatment:
Immediate cessation of the triggering stimulus
- Immediate removal of pressure to the globe of the eye or surrounding orbital tissues can terminate the reflex
Prevention:
Anesthetic agents can be used to help decrease OCR occurrence
- Pretreatment with IV anticholinergics: Atropine or glycopyrrolate
- Blocking peripheral muscarinic receptors of the heart and causes increased firing at the sinoatrial node as well as conduction through the AV node. This opposes the vagal response, or the efferent limb, of the OCR)
- Ketamine (stimulation of sympathetic activity counteracting vagal stimulation caused by OCR)
- Retro/peribulbar block with xylocaine hydrochloride to block the ciliary ganglion (blunting the afferent limb of the reflex arc can decrease OCR occurrence)