BMJ Case Rep: first published as 10.1136/bcr-2022-252692 on 7 February 2023. Downloaded from http://casereports.bmj.
com/ on February 8, 2023 at Universiti Malaysia Sabah. Protected
1
Faculty of Medicine and Health
Sciences, Universiti Malaysia
Sabah, Kota Kinabalu, Malaysia
2
Department of Anaesthesia and
Intensive Care Unit, Hospital
Universiti Sains Malaysia, Kota
Bahru, Malaysia
3
Department of Neurosciences,
School of Medical Sciences,
Hospital Universiti Sains
Malaysia, Kota Bahru, Malaysia
Correspondence to
Dr Tat Boon Yeap;
​boontat@​ums.e​ du.​my
Accepted 1 February 2023
© BMJ Publishing Group
Limited 2023. No commercial
re-­use. See rights and
permissions. Published by BMJ.
To cite: Yeap TB,
Ab Mukmin L, Ang SY,
et al. BMJ Case Rep
2023;16:e252692.
doi:10.1136/bcr-2022-
252692
Perianaesthetic challenges in patients undergoing
vagus nerve stimulation (VNS) placement
Tat Boon Yeap ‍ ‍,1 Laila Ab Mukmin,2 Song Yee Ang,3 Ab Rahman Ghani3
SUMMARY
Patients with medically refractory epilepsy (MRE) are
indicated for vagus nerve stimulation (VNS) placement.
Anaesthesia for VNS placement is extremely challenging
and requires several considerations. We present a man
in his 20s with MRE who successfully underwent VNS
placement. We review the mechanism of action of VNS,
anaesthetic challenges and measures to prevent seizures.
BACKGROUND
Vagus nerve stimulation (VNS) was approved by
the US Food and Drug Administration (USFDA)
in the year 1997 as an adjunct for the treatment
of medically refractory epilepsy (MRE).1 VNS had
been proven to successfully reduce patients’ depen-
dency to multiple antiepileptic drugs (AEDs), which
may expose them to harmful side effects. We hereby
discuss the postulated mechanism of action of VNS,
anaesthetic challenges and measures to prevent
seizures in a patient with MRE.
CASE PRESENTATION
A man in his 20s developed MRE after a chronic
herpes encephalitis infection since 10 years ago.
His generalised tonic–clonic (GTC) seizure became
more frequent for the past 2 years despite on four
AEDs, which consist of clobazam, lamotrigine,
perampanel and levetiracetam at maximal doses. He
claimed to have GTC seizure almost once a week,
which was self-­ aborted. In addition, our patient
also claimed to develop aura of which he described
seeing flashes of lights and hearing weird sounds a
few minutes before the onset of the GTC seizure.
However, he denied any triggering factors for the
seizures. He developed post-­ictal drowsiness with
occasional urinary incontinence. His conscious-
ness recovered fully approximately 15 min after the
seizure.
On clinical examination, our patient was alert and
conscious with a blood pressure (BP) of 109/72 mm
Hg, heart rate of 82 beats/min, respiratory rate of 16
breaths/min and oxygen saturation of 100% under
room air. He did not have any significant neurolog-
ical deficit apart from poor cognitive function. He
scored 17/30 in the Mini Mental State Examination
with deficits in the aspects of orientation, attention,
verbal memory, comprehension and visuospatial
skills. Other systemic examinations were normal.
INVESTIGATIONS
His serum biochemical and electrolytes were within
normal values. The cerebrospinal fluid (CSF) PCR
was positive for herpes simplex virus.
Yeap TB, et al. BMJ Case Rep 2023;16:e252692. doi:10.1136/bcr-2022-252692
Case report
His electroencephalogram (EEG) showed bilat-
eral temporal spike and generalised slowing. The
latest MRI of the brain showed volume losses with
encephalomalacic changes over bilateral temporal
regions.
DIFFERENTIAL DIAGNOSIS
Our provisional diagnosis for him was MRE
secondary to previous chronic herpes encephalitis
infection as evidenced by his biochemical and radio-
logical investigations. In addition, herpes encepha-
litis usually involved the limbic systems especially
the medial temporal and orbitofrontal lobes, which
predispose the patient to epilepsy.
Other differential diagnoses are bacterial and
autoimmune meningitis. However, these are not
possible as the CSF PCR is suggestive of viral
infection.
TREATMENT
by copyright.
Due to his MRE, our patient was scheduled for an
elective left VNS placement under general anaes-
thesia (GA). High-­risk consent was obtained from
the patient, including for this publication. Two
18-­gauge cannulas were inserted at his right and
left dorsum on the eve of the surgery. He was fasted
for 8 hours and maintained on intravenous normal
saline 0.9% drips before being pushed to the oper-
ating room. All his oral AEDs were continued on
the morning of the surgery. He was carefully placed
on the operating table with standard anaesthetic
monitoring such as capnography, non-­invasive BP,
ECG and pulse oximetry.
After preoxygenation with 100% oxygen for
5 min, GA was induced with intravenous fentanyl 2
µg/kg, propofol 2 mg/kg and rocuronium 1 mg/kg.
His trachea was gently intubated with a size 8 mm
endotracheal tube (ETT) and anchored at 21 cm at
the lips. A bispectral index (BIS) monitor was put
on his right forehead to monitor the depth of anaes-
thesia. His right radial artery was cannulated for
invasive BP and serum biochemistry monitoring. A
nasopharyngeal temperature probe was inserted to
ensure normothermia. The patient’s eyes were care-
fully padded with eye ointment to prevent expo-
sure keratitis. His anaesthesia was maintained with
the use of targeted controlled infusion (TCI) of
remifentanil and propofol at the range of 2.5–5 ng/
mL and 3–4.5 µg/mL, respectively. These were
titrated to achieve BIS values of 40–60. In antici-
pation of perioperative bradycardia, transcutaneous
pacing electrode pads were placed below the right
clavicle and apex of the heart which were then
connected to an external pacemaker. To minimise
1

Case report
Figure 1 The patient’s neck is slightly rotated to the right during
vagus nerve stimulation placement.
electromagnetic interference with the VNS, we used bipolar
electrocautery forceps and placed the grounding plate on the
patient’s right thigh.
His neck was extended and rotated slightly to the right for VNS
implantation (figure 1). A collar-­like incision was made approx-
imately 3 cm above the left clavicle, at the triangle between the
two heads of the sternocleidomastoid muscle. This was to ensure
adequate exposure to harvest a long non-­ branching cervical
segment of the left vagus nerve. The vagus nerve was identified
and dissected with the use of microscope. The VNS electrode
was placed around the vagus nerve and tunnelled to the left
infraclavicular pouch, which was then connected to the pulse
generator. His VNS was immediately paced at 1.5 mA with the
frequency of 20 Hz and ‘on time’ of 30 s.
The entire 2-­ hour surgical procedure was uneventful. The
patient’s haemodynamic profiles were stable, and bleeding was
estimated at 150 mL. An arterial blood gas prior to his extu-
bation at a fraction of inspired oxygen of 40% showed pH of
7.39, partial pressure of oxygen of 137 mm Hg, partial pressure
of carbon dioxide (PaCO2) of 36 mm Hg and bicarbonate of
21.3 mmol/L. The serum potassium, sodium and calcium levels
were within normal values. Intravenous sugammadex 2 mg/kg
was used as our reversal agent of choice. He was safely extu-
bated and sent to the neurocritical care unit (NCU) for close
monitoring. His oral AED was immediately commenced postop-
eratively. His pain was controlled with the usage of intravenous
paracetamol and parecoxib. He did not develop any immediate
neck haematoma, stridor, nor hoarseness of voice. He was
discharged home 2 days later.
OUTCOME AND FOLLOW-UP
Three months after the procedure, our patient claimed to have
developed only one short episode of mild focal seizure, which
was controlled with VNS. Upon review, his AEDs were weaned
to lamotrigine, clobazam and levetiracetam. At the ninth month
after placement, his AEDs were further weaned to lamotrigine
only with a well-­controlled seizure occurrence.
2 Yeap TB, et al. BMJ Case Rep 2023;16:e252692. doi:10.1136/bcr-2022-252692
BMJ Case Rep: first published as 10.1136/bcr-2022-252692 on 7 February 2023. Downloaded from http://casereports.bmj.com/ on February 8, 2023 at Universiti Malaysia Sabah. Protected
DISCUSSION
Seizure is characterised by a sudden transient clinical behavioural
change due to excessive abnormal firing of the brain neurons.2
Epilepsy is a brain disorder due to unprovoked repeated
seizures.3 AED is the mainstay of treatment for patients with
epilepsy. However, AED may not be effective in patients with
MRE. It is defined as patients who do not achieve good seizure
control with the usage of three monotherapy AED trials and at
least two polytherapy trials within the first 2 years since begin-
ning of treatment.4
MRE is usually diagnosed after undergoing detailed clinical
neurological assessment and investigations such as EEG, brain
positron emission tomography and MRI.5 Epilepsy surgery is
indicated if the pathophysiology is understood and both EEG
and MRI show focal lesions such as mesial temporal sclerosis,
tuberous sclerosis and cortical dysplasia.6 7 VNS is an option in
patients with MRE with bilateral multiple foci and idiopathic
generalised epilepsy secondary to cerebral palsy and intracranial
infection.8
In the 1980s, Zabara discovered that VNS could eliminate
seizures in dogs.9 Penry and Dean were the first to implant vagal
stimulating devices onto four humans with intractable partial
seizures in 1988.10 They found good seizure control on 75%
of their patients with VNS. In 1997, the USFDA approved the
usage of VNS as an adjunct to the treatment of MRE.1 Several
researches in the year 2011 showed that VNS reduced the
frequency of seizures by 50% within the first year of implanta-
tion.11 12
About 80% of the vagus nerve fibres are afferent, which carries
somatic and visceral impulses to the nucleus tractus solitarus
by copyright.
(NTS).13 The remainder of the vagus nerve is parasympathetic
efferents, which connects to the heart, lungs, gastrointestinal
system and motor to the larynx and pharynx. Electrical current
via the VNS stimulates the vagus nerve, which will create action
potentials that regulate cerebral neuronal excitability, either
through activation of the limbic, noradrenergic neurotransmitter
systems or brainstem arousal systems via the NTS (figure 2).14
The VNS system consists of a platinum electrode, which is
wrapped around the left vagus nerve, a lead wire and pulse
generator (figure 3).15 The latter delivers an electrical current
based on programmed parameters and is placed onto the
patient’s chest below the ipsilateral clavicle. The parameters of
the generator include output current, frequency, and stimula-
tion on-­time and off-­time, similar to the cardiac pacemaker. The
generator provides an electrical current of 1–2 mA for 0.5 ms,
which is repeated over an interval of 20–30 Hz for 30 s every
5 min throughout the day. A magnet, when placed on top of the
generator, provides additional stimulation to allow companions
or patients to activate it to stop an impending aura or seizure.
GA with intermittent positive pressure ventilation is admin-
istered to patients who undergo VNS implantation. Patients are
positioned supine with the neck slightly rotated to the right and
the surgical incision is performed within the left cervical portion
of the vagus nerve. The right vagus nerve, which innervates the
sinoatrial node and contains dense cardiac efferent fibres, is
avoided as stimulation may cause severe myocardial complica-
tions such as bradycardia and asystole.16
The principles of anaesthesia during VNS placement are to
avoid seizure-­ triggering agents, ensure stable haemodynamic
and immediate management of perioperative airway complica-
tions. Patients should be assessed on the seizure type, frequency
and duration, in addition to its triggering factors and presence
of aura. Gingival hyperplasia, a sequela to chronic phenytoin
 BMJ Case Rep: first published as 10.1136/bcr-2022-252692 on 7 February 2023. Downloaded from http://casereports.bmj.com/ on February 8, 2023 at Universiti Malaysia Sabah. Protected
Case report

Figure 2 Mechanism of action of VNS (figure was illustrated by TBY). DR, dorsal raphe; LC, locus coeruleus; PPN, pedunculopontine nucleus; VNS,
vagus nerve stimulation.

exposure, can predispose to airway trauma during laryngoscopy
and intubation. Phenytoin, phenobarbitone and carbamaze-
pine are potent cytochrome p450 enzyme inducers and accel-
erate the metabolism of intravenous induction agents, opioids
and muscle relaxants.17 Thus, patients will require higher doses
of such agents intraoperatively. In addition, AED can cause
various haematological abnormalities such as anaemia, throm-
bocytopenia, coagulopathies and purpura. These values should
be corrected prior to VNS placement. AED is continued on the
morning of the surgery to help control seizures that may occur
perioperatively.
by copyright.
It is vital to ensure stable intraoperative haemodynamics during
VNS placement. As the patient’s neck will be slightly rotated
to the right, a re-­enforced ETT is useful to prevent kinking or
compression which may lead to hypoxaemia and hypercapnoea.
Intra-­arterial catheters are required for precise blood gases and
pressure monitoring. Hypotension, hypocapnoea, hypoxaemia,
hyperthermia, hypernatraemia, hyponatraemia, hypocalcaemia,
hypomagnesaemia and hypoglycaemia should be avoided as they
may lower seizure threshold18–20 (table 1). Hypocapnoea, with
PaCO2 of <35 mm Hg, decreases the alpha and beta twitches
and induces a synchronous epileptiform delta activity in the
EEG.21 These changes are more common to occur in children
with epilepsy than in adults. Patients should be maintained euvo-
laemic throughout and rapid resuscitation with blood products
in the event of accidental trauma to the common carotid artery
and internal jugular vein. Surgical manipulation to the left vagus
nerve may precipitate arrhythmia, bradycardia and heart block.

Table 1 Factors that may trigger perioperative seizures

Pharmacological Non-­pharmacological
Inhalational agents such as nitrous oxide, Hypocapnoea
enflurane, sevoflurane and desflurane
Intravenous agents such as etomidate Hypoxaemia
and ketamine
Local anaesthetic agents in toxic doses Hypotension
Opioids in supramaximal doses and Electrolyte imbalances such as hypo/
pethidine hypernatraemia, hypomagnesaemia and
hypocalcaemia
Prolonged infusion of atracurium Hypoglycaemia
Anticholinergics such as atropine and Hyperthermia
scopolamine
Figure 3 Vagus nerve stimulation (VNS) electrodes wrapped around
Pain
the vagus nerve of our patient.
Yeap TB, et al. BMJ Case Rep 2023;16:e252692. doi:10.1136/bcr-2022-252692 3

Case report
Thus, it is vital to ensure that an external pacemaker is within
reach when the need arises intraoperatively. Extra surgical
precautions are needed during the usage of electrocautery to
avoid damage to the VNS. Monopolar cautery must be avoided
at all times and short bursts of bipolar diathermy are encouraged.
In addition, the grounding pads for the electrocautery should be
placed as far away as possible from the pulse generator.
Anaesthetic agents have variable effects on seizure threshold.
Intravenous induction drugs, such as propofol and thiopentone,
have depressant EEG effects thus decreasing the likelihood of
seizures.21 Propofol elevates the seizure threshold potentials
and is safe for patients with MRE. Ketamine and etomidate may
trigger seizure activities, thus must be avoided. EEG epilepti-
form activities are seen from the administration of supramax-
imal doses of opioids. Opioids such as alfentanil (50–75 µg/kg),
fentanyl (>200 µg/kg) and sufentanil (>40 µg/kg) have induced
cortical seizure activities in animal models.19 Large doses of
remifentanil (bolus of 1 µg/kg with subsequent infusion of 1–3
µg/kg/min) activated the human limbic system and induced
tonic–clonic seizures.22 Lower doses of fentanyl, alfentanil and
remifentanil (<1 µg/kg/min) possess good anticonvulsant activi-
ties. Pethidine should be avoided as its metabolite, norpethidine,
is a proconvulsant. As VNS is minimally invasive, higher opioid
usage is not indicated as a mode of analgesia. TCI of remifentanil
and propofol possesses good anticonvulsive properties in the
expense of maintaining adequate cerebral perfusion pressure,
cerebral blood flow and burst suppression.23 Several studies had
Table 2 Perioperative complications of VNS placement
Acute Delayed
Peritracheal haematoma Pharyngitis
Bleeding Cough
Left vocal cord paralysis OSA
Hoarseness of voice Infection
Aspiration pneumonitis Headache
Cardiovascular: bradycardia, asystole, complete
atrioventricular block and hypotension
Seizures
OSA, obstructive sleep apnoea; VNS, vagus nerve stimulation.
Patient’s perspective
I am fortunate to have undergone a safe VNS placement in this
hospital which is well managed by experienced neurosurgeons
and neuroanaesthesiologists. With their safe hands, I am now a
happy man and not having to consume so many medications for
my epilepsy. My seizure is not frequent after VNS and able to do
my activities of daily living comfortably. Thank you.
Learning points
► Patients with medically refractory epilepsy are indicated for
vagus nerve stimulation (VNS).
► VNS placement is a high-­risk surgery that is often associated
with severe life-­threatening cardiorespiratory complications.
► Anaesthesiologists must avoid physiological derangements
and drugs that reduce seizure thresholds.
► Targeted controlled infusion of remifentanil and propofol
is highly recommended for induction and maintenance of
anaesthesia for such patients.
4 Yeap TB, et al. BMJ Case Rep 2023;16:e252692. doi:10.1136/bcr-2022-252692
BMJ Case Rep: first published as 10.1136/bcr-2022-252692 on 7 February 2023. Downloaded from http://casereports.bmj.com/ on February 8, 2023 at Universiti Malaysia Sabah. Protected
reported that isoflurane is safe to be administered in patients
with MRE. However, epileptiform activities have been demon-
strated in a dose-­dependent manner among inhalational agents
such as desflurane, sevoflurane and enflurane in both patients
with epilepsy and those without epilepsy during surgical anaes-
thesia.24 Nitrous oxide was shown to provoke seizures in cats,
but it had not been replicated in humans.25 Generally, depo-
larising and non-­ depolarising neuromuscular blocking agents
have no effects on seizure threshold potentials. Prolonged usage
of atracurium may lead to the accumulation of its metabolite,
laudanosine, which had been shown to cause EEG and clinical
seizures in animals.26
Common postoperative complications of VNS are seizures,
lower facial muscle paralysis and peritracheal haematoma27
(table 2). The latter is an airway emergency and should be
urgently managed by surgical exploration. Damage to the vagus
nerve and its branches, such as the recurrent laryngeal and supe-
rior laryngeal nerves, causes hoarseness of voice and left vocal
cord paralysis, respectively. Direct laryngoscopy is useful to
diagnose these life-­threatening complications and urgent intuba-
tion is warranted. Seizures should be considered in patients with
delayed awakening from anaesthesia and changes in postopera-
tive mental status. The reported cardiac complications of intra-
operative stimulation include bradycardia, asystole, complete
heart block, dysrhythmia and hypotension. They resolve spon-
taneously after halting the stimulation and responded well to
intravenous epinephrine and atropine.27–29
Chronic VNS stimulation may lead to various types of laryn-
gopharyngeal dysfunction such as voice alteration, pharyn-
gitis, throat discomfort, obstructive sleep apnoea (OSA) and
by copyright.
dyspnoea.30 Worsening of OSA has been reported in patients
with VNS.31 Upper airway obstruction may occur due to periph-
eral stimulation of vagal afferents which will activate motor
efferents, resulting in altered neuromuscular transmission to
the laryngeal and pharyngeal muscles.32 33 The use of VNS
may lead to a decrease in oxygen saturation, air flow and tidal
volume during sleep, resulting in an increase in apnoea–hypop-
noea index. Thus, extreme caution should be exercised in obese
patients with moderate-­to-­severe OSA.
We were fortunate that the VNS placement on our patient
was uneventful. All oral AEDs were served prior to surgery for
adequate seizure control. We administered TCI of propofol and
remifentanil as our choice of anaesthesia. In addition, we also
avoided physiological derangements and drugs that may trigger
seizures intraoperatively. His oral AED was commenced immedi-
ately in the NCU to prevent seizures. Usage of VNS was proven
to be effective as he had good seizure control and his AEDs were
reduced by 50% after 9 months of implantation.
Acknowledgements We would like to thank the patient for his kindness in
allowing us to share and publish this important achievement in neuroanaesthesia.
Contributors TBY and LAM were the anaesthesiologists in charge of the patient.
SYA and ARG were the neurosurgeons involved in the surgery. TBY is the main and
corresponding author for this manuscript.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-­for-­profit sectors.
Competing interests None declared.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
Case reports provide a valuable learning resource for the scientific community and
can indicate areas of interest for future research. They should not be used in isolation
to guide treatment choices or public health policy.

ORCID iD
Tat Boon Yeap http://orcid.org/0000-0002-2517-597X
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BMJ Case Rep: first published as 10.1136/bcr-2022-252692 on 7 February 2023. Downloaded from http://casereports.bmj.com/ on February 8, 2023 at Universiti Malaysia Sabah. Protected
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