J. Cranio-Max.-Fac.Surg.
18 (1990) 359
J. Cranio-Max.-Fac. Surg. 18 (1990) 359-360
© Georg Thieme Verlag Stuttgart. New York
Bradycardia and the
Trigeminal Nerve
Neal A. Barnard, Roger Bainton
Regional Oral and Maxillofacial Unit Broadgreen Hospital, Liverpool,
England
Submitted 26. 4. 1990; accepted 26. 6. 1990
Introduction
The oculocardiac reflex was first described simultaneously
by Aschner (1908) and Dagnini (1908), and has been well
documented in relation to stimuli in and around the orbit
(Dewar and Wishart, 1976; Kerr and Vance, 1983; Stott,
1989). Cardiac dysrhythmia arising from other sites in the
head and neck have been sporadically reported (Kaufrnan,
1965; Robideaux, 1978), with a renewed interest in the ref-
lex due to the advent of modern anaesthetic agents (Arndt
et al., 1984; Milligan and Beers, 1985; Inoue and Reichelt,
1987). The common factor is the stimulation of facial struc-
tures innervated by the trigeminal nerve.
Case Reports
Case report 1
A 26-year-old woman, weight 60 kg., was anaesthetised for
a Le Fort I osteotomy for facial disproportion. She had no
history of cardiovascular or other medical problems.
Premedication consisted of 10 mg diazepam, given orally,
and anaesthesia was induced with 300 mg sodium thiopen-
tone. Vecuronium 7 mg was administered and naso-endo-
tracheal intubation effected. Anaesthesia was maintained
using enflurane 1% in a 66 % nitrous oxide mixture, she
was also given 2 mg droperidol at the commencement of
surgery. ECG and blood pressure were both monitored.
The pulse rate was 70 beats per minute and the blood pres-
sure 130/80 mm Hg after induction.
At 30 minutes into the operation a further dose of 2 mg of
vecuronium was given intravenously. The operation pro-
ceeded uneventfully for a further ten minutes until the max-
illary disimpaction forceps were applied to the maxilla and
the down-fracture of the maxilla commenced. The ECG
monitor showed a rapidly progressive bradycardia to 25
beats per minute with a demonstrable drop in blood pres-
sure. The traction on the maxillary fragment was immedi-
ately stopped. Atropine sulphate 0.6 mg was administered
intravenously and the pulse rate rose progressively to 96
beats per minute. The blood pressure also recovered to a
satisfactory level.
The maxillary fragment was placed in the new position and
plated without incident. No further problems were experi-
enced and the patient made a full recovery. A postoperative
ECG was normal.
Summary
A review of the literature suggests that the oculocardiac
reflex is part of a wider phenomenon involving any
structure supplied by the trigeminal nerve. This can
lead to potentially fatal complications in maxillofacial
surgery. A review of the literature is discussed and two
further cases are reported.
Key words
Bradycardia - Trigeminal nerve - Craniofacial surgery
Case report 2
A 62-year-old Caucasian male, weight 68 kg, was admitted
to hospital following a fall from a ladder. He had sustained
the following fractures:
A depressed fracture of the left zygomatic complex with
distraction of the fronto-zygomatic suture and an associat-
ed blow-in fracture of the lateral orbital wall. The latter was
confirmed by computed tomographic scan. The patient
had no medical history of note. Examination of the cardio-
vascular system revealed that the pulse was 76 beats per mi-
nute, the blood pressure was 140/80 mm Hg and the pre-
operative electrocardiogram was normal.
The patient was not pre-medicated before operation.
Anaesthesia was induced with 250rag thiopentone and
muscle relaxation was attained with 8 mg of vecuronium.
Anaesthesia was maintained with 66 % nitrous oxide and
33 % oxygen plus 1 to 0.5 % isoflurane and the patient was
ventilated via an endotracheal tube. Muscle relaxation was
maintained throughout the operation with 3 mg vecuroni-
um administered half hourly and alfentanyl 250 mcg was
given intravenously for analgesia. The ECG and blood pres-
sure were monitored throughout. The pulse rate was 95
beats per minute and the blood pressure 160/90 mm Hg at
induction.
A bitemporal flap approach was employed for access to the
fronto-zygomatic suture and lateral orbital wall. The peric-
ranium was mobilised bilaterally by blunt dissection and as
the lateral wall fracture was mobilised, a rapidly progressive
bradycardia developed to 20 beats per minute. The systolic
blood pressure also showed a significant drop. The dissec-
tion was stopped immediately and 0.5 mg glycopyrronium
was administered intravenously and the heart rate accelerat-
ed to 90 beats per minute. These conformed to a normal si-
no-atrial nodal rhythm. There was no further episode of
dysrhythmia when the zygomatic complex fracture was re-
duced and plated nor when a sheet of xenoderm was
placed to repair the left lateral wall and floor defects re-
spectively. The operation was completed uneventfully and
the heart rate and systolic arterial pressure remained stable.
The patient made an uneventful recovery and was dis-
charged from hospital 3 days postoperatively.
360 J. Cranio-Max.-Fac. Surg. i8 (1990)
Discussion and Conclusions
These two cases demonstrate a reflex bradycardia similar to
the oculocardiac reflex but in the first case stimuli did not
directly involve the orbit or adnexa. Loewinger et al. (1987)
and Shearer and Wenstone (1987) described a bradycardia
during elevation of zygomatic complex fractures, whilst
Bainton and Lizi (1987) described cardiac asystole in the
treatment of an isolated zygomatic arch fracture. Recently
cardiac asystole has also been reported following the reflec-
tion of bitemporal flaps (Bainton et al. 1990), and a Le Fort
I osteotomy (Ragno et al., 1989). Similarly to case 1 a
bradycardia with ventricular ectopic beats occuring concur-
rently with manipulation of the maxilla during a maxillary
osteotomy has been reported by Shelley and Church
(1988). Other reports of bradycardia include diathermy to
the tentorium cerebelli (Hoptains, 1988), foley catheter ex-
pansion of the nasolabial groove and during obliteration of
the frontal sinus (Stott, 1989).
Although the sites of stimulation precipitating this pheno-
menon are diverse, they all represent examples of a trigemi-
no-vagal reflex rather than the narrower definition of the
oculocardiac reflex. A possible anatomical pathway for the
former was recently reiterated by Scott (1989), employing
the original description of Katz and Bigger (1970). How-
ever, this description applies exclusively to the oculo-card-
iac reflex. A more likely explanation regarding the anatomi-
cal pathways for the trigemino-vagal reflex has been postu-
lated by Bainton et al. (1990), which may explain why card-
iac dysrythmias can potentially occur following stimulation
of any branch of the trigeminal nerve. The stimuli triggering
the reflex are probably pain and or proprioception. The re-
sponse of the former may be potentiated by fentanyl (Bain-
ton et al., 1990) but this effect has only been previously re-
ported in unanaesthetised dogs (Arndt et al., 1984). A pre-
operative dose of atropine sulphate has been shown to be
largely ineffective in the prevention of this reflex but atro-
pine sulphate or glycopyrrolate administered intravenously
at the time of induction of anaesthesia has been demon-
strated to be effective in abolishing the reflex (Mirateur and
Jones 1982).
The diverse head and neck stimuli which may cause cardiac
dysrhythmias lead the authors to the view that the term
oculocardiac reflex does not reflect the total extent of this
potentially fatal reflex and thus should be renamed the tri-
gemino-vagal reflex.
N. A. Barnard, R. Bainton: Bradycardia and the Trigeminal Nerve
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Mr. N. A. Barnard
Dept. Oral and Maxillofacial Surgery
Frenchay Hospital
Bristol BS 161LE
England