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Review Article
Cranial nerve injuries with supraglottic airway devices: a
systematic review of published case reports and series
V. Thiruvenkatarajan,1,2 R. M. Van Wijk3,4 and A. Rajbhoj1,2
1 Staff Specialist Anaesthetist, 3 Head, Department of Anaesthesia, The Queen Elizabeth Hospital, Woodville, SouthAustralia, Australia2 Clinical Senior Lecturer, 4 Associate Professor, Discipline of Acute Care Medicine, The University of Adelaide, Adelaide,South Australia, Australia
SummaryCranial nerve injuries are unusual complications of supraglottic airway use. Branches of the trigeminal, glossopharyn-
geal, vagus and the hypoglossal nerve may all be injured. We performed a systematic review of published case reports
and case series of cranial nerve injury from the use of supraglottic airway devices. Lingual nerve injury was the most
commonly reported (22 patients), followed by recurrent laryngeal (17 patients), hypoglossal (11 patients), glossopha-
ryngeal (three patients), inferior alveolar (two patients) and infra-orbital (one patient). Injury is generally thought to
result from pressure neuropraxia. Contributing factors may include: an inappropriate size or misplacement of the
device; patient position; overinflation of the device cuff; and poor technique. Injuries other than to the recurrent lar-
yngeal nerve are usually mild and self-limiting. Understanding the diverse presentation of cranial nerve injuries helps
to distinguish them from other complications and assists in their management..................................................................................................................................................................
Correspondence to: V. Thiruvenkatarajan
Email: [email protected]
Accepted: 22 September 2014
Presented at the Australian and New Zealand College of Anaesthetists’ Annual Scientific Meeting, Singapore, May
2014.
IntroductionThe classic laryngeal mask airway (cLMA, LMA North
America, San Diego, CA, USA) was invented by Dr
Archie Brain in 1981 and introduced into clinical prac-
tice in 1988 [1, 2]. Since that time, other airway
devices that do not pass through the larynx have been
invented, and these and the original LMA are referred
to as supraglottic airway devices. They are widely used
in day-to-day practice, being used in roughly 50% of
all general anaesthetic procedures [2].
The morbidity associated with the use of supra-
glottic airway devices is largely defined by minor phar-
yngolaryngeal complications such as: sore throat (17–
42% of patients) [3]; soft tissue abrasion (16–32%) [4];
hoarseness and dysphagia. Cranial nerve injury after
the use of a supraglottic airway device is an unusual
but more serious complication. So far, injuries of lin-
gual, inferior alveolar, infra-orbital, glossopharyngeal,
recurrent laryngeal and hypoglossal nerves have been
reported. The true incidence of these injuries is not
known; we suspect many are not reported. We have
conducted a systematic review of all published case
reports and case series of cranial nerve injury following
the use of supraglottic airway devices. The aim of this
review is to analyse and summarise the features of cra-
nial nerve injuries associated with supraglottic airway
344 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 doi:10.1111/anae.12917
devices, with particular emphasis on contributing
factors.
MethodsWe searched PubMed and Embase for material pub-
lished up to April 31, 2014, and identified case reports
and case series mentioning cranial nerve injuries associ-
ated with supraglottic airway devices (details of the
search strategy are presented in the Appendix). The
search was not limited to a particular start date and we
did not impose a restriction on language of publication.
The bibliographies of the identified publications were
hand-searched for additional reports. We included
reports of both adults and children, as there seems to be
no clear evidence that the mechanisms of nerve injury
differ between these two groups. To be included, the
reports had to describe and confirm the clinical evidence
of cranial nerve injury in association with the use of any
type of supraglottic airway device. Two authors working
independently extracted the following data: age, sex and
weight of the patient; size and type of device inserted;
use of nitrous oxide; cuff volume and pressure; times of
onset and resolution of symptoms; management; and
any contributing factors.
ResultsOur searches generated a total of 164 articles from
PubMed and 191 from Embase. After excluding 45
duplicates, 312 reports were left. Of these, there were
53 reports meeting the eligibility criteria (Fig. 1),
reporting a total of 56 patients. The reports were pub-
lished between 1994 and 2014; our analysis of four
reports was restricted to the abstract as we were unable
to secure translations. Patient ages ranged from
9 months to 75 years.
Recurrent laryngeal nerve damageOur review identified 16 cases of recurrent laryngeal
nerve injury [5–19]. Of these, 13 were reported with
the cLMA and its variants [5–16], two with the Pro-
Seal LMATM [17, 18] and one with the Air-QTM LMA
[19] (Table 1).
Of all the cranial nerve injuries, damage to the
recurrent laryngeal nerve was most likely to present
with significant morbidity. Uniquely among the nerve
injuries described in this review, it may present both
intraoperatively and postoperatively. The recurrent lar-
yngeal nerve ascends in the tracheo-oesophageal
groove and enters the larynx by passing under the
lower border of the inferior constrictor muscle at the
apex of the piriform fossa [5]. When correctly placed,
the tip of the LMA cuff is positioned at the inferior
border of the hypopharynx, against the upper oesopha-
geal sphincter at the level of the C6–C7 vertebral inter-
space (Fig. 2). The nerve is vulnerable to injury as it
enters the larynx, where it can be pinched against the
cricoid cartilage (Figs. 2 and 3). Unilateral paralysis
results in the vocal cord’s resting in the paramedian
position. In this situation, the laryngeal inlet will be
adequate and airway obstruction is unlikely. However,
inadequate glottic closure might result in hoarseness,
and laryngeal incompetence may lead to impaired
coughing and risk of aspiration. Bilateral palsy may
cause the vocal cords to be positioned in the midline,
with narrowing of the glottic aperture. This may pres-
ent as dyspnoea or inspiratory stridor, and occasionally
severe respiratory distress [20]. Respiratory difficulty,
requiring intubation or tracheostomy, and permanent
voice impairment are the most severe complications.
In the cases reported, it was sometimes difficult to
establish the diagnosis. For instance, the authors of
one report could not ascertain whether the vocal cord
palsy (presenting as voice impairment) after LMA use
was due to the device, or to the presence of a cervical
spine osteophyte compressing the nerve close to the
trachea and oesophagus [21]. Furthermore, vocal cord
palsy after the use of supraglottic airway devices clo-
sely resembles arytenoid cartilage subluxation and is
thus likely to be under-diagnosed [22, 23].
In the 16 cases we reviewed, the time of presenta-
tion varied from immediately after the insertion of the
LMA to up to 48 h later. Hoarseness was the most
common manifestation, followed by dysphagia and
dysphonia. Four reports documented bilateral injury.
Two patients required tracheostomy [9, 17]; one pre-
sented intra-operatively, the other 2 h after removal
[9]. A child required mechanical ventilation [12]. The
fourth patient developed features of unilateral paralysis
(aphonia and difficulty in coughing) but was found to
have bilateral paralysis when inspected through the fi-
breoptic bronchoscope [16]. Both the patients in
whom the Pro-Seal was used also needed tracheosto-
© 2014 The Association of Anaesthetists of Great Britain and Ireland 345
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
mies; one was performed in the operating room at the
time of the injury; the other required the procedure
two weeks after the anaesthetic, following aspiration
pneumonia. Co-existing disorders in the form of spi-
nocerebellar ataxia [17] and CREST (calcinosis, Ray-
naud’s phenomenon, oesophageal dysmotility,
sclerodactyly and telangiectasia) with Sjogren’s syn-
drome [18] were present in these patients. Flexible fi-
breoptic bronchoscopy or nasal endoscopy may help
in the immediate diagnosis of the more serious bilat-
eral presentations and assist in identifying conditions
that might require urgent treatment such as mucosal
trauma and arytenoid dislocation. Electromyography,
CT scan, MRI scan or video stroboscopy may also help
in distinguishing arytenoid dislocation [24] and other
causes of cord palsy. Of the 16 patients, five were
managed conservatively with recovery times varying
from 1 h up to 19 months. Partial recovery was noted
in four patients. Laryngoplasty, thyroplasty and
mechanical ventilation were required in three separate
patients [6, 7, 12]. Persisting voice damage with partial
recovery of vocal cord function was noted in five
patients [6, 7, 13, 14, 17].
Cuff pressure was described in only one patient
[17]. Cuff volume was mentioned in nine patients and
all except one [13] had an appropriate volume. Cuff
overinflation was postulated in two reports [13, 18].
Other contributory factors suggested were: incorrect
size of device for the patient [6, 8, 13]; the use of lido-
caine jelly [13, 16]; long duration of surgery [9]; poor
insertion technique [22]; reduced mucosal circulation
[17, 18] and activation of the inflammatory cascade
[14, 17] (Table 4).
Hoarseness after supraglottic airway use cannot
always be attributed to transient laryngeal irritation [6];
the possibility of recurrent laryngeal nerve injury should
always be considered. Persistent cough, speech impair-
ment or respiratory compromise warrant careful
examination and follow-up with referral to an otolaryn-
gologist [7]. Management options other than conserva-
tive treatment include voice therapy, glucocorticoids
and surgical interventions for persisting palsies. Finally,
though supraglottic airway may be preferable to tracheal
intubation in professional voice users, such patients
should be informed pre-operatively about this recurrent
laryngeal nerve injury and its consequences [5].
Records identified through manual search (n = 3)
Duplicates removed (n = 45)
Relevant articles screened
(n = 313)
Excluded: Based on title and abstract (n = 222)
Full text articles assessed for eligibility (n = 91)
Excluded (n = 38)Not meeting theInclusion criteria (n = 37)Unable to get Japanese abstract (n = 1)Reports included (n = 53)
(Includes abstract only data from 3 Japanese and one Danish report)
Trigeminal nerve Reports (n = 23)Patients (n = 25)Lingual (n = 22)Inferior alveolar (n = 2)Infra-orbital (n = 1)
Recurrent laryngeal nerveReports (n = 16)Patien ts (n = 17)
Hypoglossal nerveReports and patients (n = 11)
Glossopharyngeal nervePatients (n = 3)
Iden
tific
atio
n S
cree
ning
Elig
ibilit
yIn
clud
ed
Number of records identified from PubMed and Embase(n = 355)
Figure 1 Flow diagram of the literature search and selection process.
346 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
Table
1Summaryof
recurrentlaryngealnerveinjuries
followinguseof
differenttypesof
supraglottic
airw
aydevice.
Reference
Age;
years/
sex
Weight;
kg
Sizeof
device
Duration
of
surgery;
min
N2O
use
Cuff
pressure/
volume
measu
red
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
Classic
LMA
Wadelek
etal.[8]
57/M
98
470
No
33ml
Unilateral
Hoarseness
dysphagia,
tongue
deviation
PACU
MRI
Few
months
Toosm
all
amask?,
Semi-supine
position
Endo
etal.[9]
63/F
48
3425
Yes
20ml
Bilateral
Shortness
ofbreath
2h
Trach
eostomy
1month
Longduration,
arytenoid
compression
Chanand
Grillone[6]
50/M
120
560
NR
NR
Unilateral
Hoarseness,
dysphonia
PACU
CTscan,
Injection
laryngoplasty
19months
(partial)
Toolargea
mask?
Bruce
etal.[10]
21/M
NR
575
Yes
NR
Unilateral
Hoarseness
2days
Conservative
5months
NR
Minoda
etal.(A
)[11]
58/F
NR
NR
NR
NR
NR
Unilateral
Hoarseness,
dysphagia
NR
NR
2months
NR
Sacks
etal.[12]
4/M
17
290
Yes
7ml
Bilateral
Inspiratory
stridor
Endofcase
Intubation,
ventilation
24h
Intra-operative
cuff
pressure
increase
Lowinger
etal.[7]
44/M
NR
450
Yes
20ml
Unilateral
Dysphonia,
aphonia
24h
Thyroplasty
18months
(partial)
NR
Brimaco
mbe
etal.[13]
74/M
83
360
Yes
35ml
Unilateral
Hoarseness,
sore
throat
Few
hours
Conservative
3months
(partial)
Poortech
nique,
toosm
alla
mask,
ove
r-inflation
ofcu
ff,
lidocainejelly
Cros
etal.[14]
19/M
67
490
Yes
20ml
Unilateral
Dysphonia,
laryngeal
inco
mpetence,
fluid
aspiration,
sore
throat
Few
hours
NR
2months
Isch
aemic
inflammatory
reaction
Cros
etal.[14]
54/M
52
360
Yes
30ml
Unilateral
Dysphagia,
hoarseness,
laryngeal
inco
mpetence
Few
hours
NR
6months
(partial)
Ove
r-inflation
ofcu
ff
Daya
etal.[5]
64/F
36
460
Yes
NR
Unilateral
Hoarseness
48h
Conservative
3months
Pressure
neuropraxia
© 2014 The Association of Anaesthetists of Great Britain and Ireland 347
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
Table
1(continu
ed)
Reference
Age;
years/
sex
Weight;
kg
Sizeof
device
Duration
of
surgery;
min
N2O
use
Cuff
pressure/
volume
measu
red
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
Lloyd
Jones
and
Hegab[15]
39/F
72
430
Yes
30ml
Unilateral
Hoarseness
2days
NR
3weeks
Pressure
neuropraxia
Inomata
etal.[16]
45/F
41
397
Yes
15ml
Bilateral
Aphonia
Immediate
Conservative
40min
Lidocainejelly
Pro-Seal
Carron
etal.[17]
67/F
60
460
No
60cm
H2O
Bilateral
Laryngeal
oedema
Intra-
operative
Trach
eostomy
NR
Reduced
muco
salblood
flow,altered
cricoarytenoid
function,
inflammatory
cascade
Kawauch
ietal.[18]
71/F
50
3117
Yes
40ml
Unilateral
Dysphagia,
hoarseness,
coughing
24h
Minitrach
eostomy
2months
(partial)
Double
the
reco
mmended
volume,
reduced
muco
salblood
flow
Air-Q
TMLM
ABlais
etal.[19]
75/F
NR
3NR
No
NR
Unilateral
Vocalco
rdbowing
toright
After
insertion
LMA
adjustment
Immediate
Mech
anical
force
PACU,po
st-anaesthesia
recovery
unit;MRI,magneticresonanceim
aging;
NR,no
trecorded;A,abstract
data.
348 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
Trigeminal nerve injuryThe three divisions of this nerve are the ophthalmic,
maxillary and mandibular. Of all the branches of the
trigeminal nerve, the lingual nerve, a peripheral branch
of the mandibular nerve, was the most commonly
injured by supraglottic airway use. The inferior alveo-
lar branch of the mandibular nerve can also be dam-
aged. The only branch of the maxillary nerve at risk is
the infra-orbital nerve [25]. We identified 25 cases of
nerve injuries related to the peripheral branches of the
trigeminal nerve (Table 2). Of these, 22 were lingual
nerve injuries [24, 26–44], two inferior alveolar [45,
46] and one infra-orbital [25].
Of the 22 lingual nerve injuries, 14 were associated
with the use of the cLMA and its variants [24, 26–37].
The Pro-Seal, LMA SupremeTM, i-gel� and COPATM
(cuffed oropharyngeal airway) had two associated inju-
ries each [38–44].
The lingual nerve lies immediately beneath the
mucosa on the inner surface of the mandible just
below the roots of the third molar tooth [37]. It then
passes forward to the side of the tongue, crossing the
hyoglossus muscle, and divides into terminal branches
that lie directly under the mucosa of the tongue. The
nerve is susceptible to injury by compression or
stretching by supraglottic airway devices at two points:
the lateral edge of the tongue base; and the medial
aspect of the inner surface of the mandible close to the
third molar [47, 48] (Figs. 2 and 4). Transient numb-
ness of the anterior tongue and altered taste perception
(dysgeusia) were the most common presentations.
Numbness at the tip and the lateral half of the tongue
can also be present, and can affect speech articulation
[49]. Symptoms can occur as early as a few minutes
after insertion to as late as 24 h. Lingual nerve injury
has to be differentiated from hypoglossal nerve dam-
age, which presents predominantly as motor weakness
of the tongue. No specialised investigations are
required but a subjective sensory assessment of the
tongue is useful, and aids in the monitoring of recov-
ery [48].
The cuff pressure was described in only three
patients [24, 25, 29]; the cuff volume was recorded in 11
patients. The contributing factors discussed included:
nitrous oxide use; malpositioning; incorrect sizing; pro-
longed duration of surgery; and chemical neuronitis
secondary to the use of wrong lubricant (Table 4).
Recovery occurred in all patients with lingual
nerve injury without specific treatment; this took from
a few hours to up to six months. Similar self-limiting
symptoms are frequently encountered after dental
Infra-orbital nerve
Lingual nerveInferior alveolarnerve
Hypoglossalnerve
Recurrent laryngealnerve
Hyoid bone
Mental nerve
C6
Figure 2 Schematic illustration of the position of a su-praglottic device in relation to the cranial nerves ofinterest.
Figure 3 Anatomical preparation of a laryngeal maskairway in situ. The cuff is inflated next to the pointwhere the thyroid and cricoid cartilages meet (arrow)where the recurrent laryngeal nerve is situated. At thislocation, the nerve enters the larynx from within thetracheo-oesophageal groove. ‘Oesoph’ denotes oesopha-gus (reproduced with permission from [21]).
© 2014 The Association of Anaesthetists of Great Britain and Ireland 349
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
Table
2Summaryof
trigem
inal
nerveinjuries
followinguseof
differenttypesof
supraglottic
airw
aydevices.
Reference
Age;
years/
sex
Weight;
kg
Size
Duration
of
surgery;
min
N2O
use
Cuff
pressure/
volume
measu
red
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
Lingualnerve
Classic
LMA
variants
Dhillonand
O’Leary
[24]
52/F
NR
460
No
<60cm
H2O
Bilateral
Numbness,
taste
disturbance
Instant
Conservative
4weeks
EBUS
induced
LMA
move
ment
ElToukhyand
Tweedie
[26]
36/F
NR
4180
No
No
Bilateral
Numbness,
taste
disturbance
PACU
Conservative
6weeks
NR
Foleyetal.[27]
21/M
79
545
No
40ml
Unilateral
Numbness,
taste
disturbance,
Few
hours
Conservative
4weeks
NR
Foleyetal.[27]
50/F
101
370
Yes
NR
Unilateral
Numbness
PACU
Conservative
4weeks
NR
In� acioetal.[28]
55/F
75
4150
NR
20ml
Bilateral
Numbness,
taste
disturbance
1h
Conservative
2weeks
Smallsize
Fidelerand
Schroeder[29]
32/F
NR
460
NR
50cm
H2O
Unilateral
Numbness,
taste
disturbance
Few
hours
Conservative
4days
TMJ
subluxa
tion
Cardoso
etal.[30]
36/F
60
3120
NR
30ml
Bilateral
Numbness,
taste
disturbance
1h
Conservative
3weeks
Smallsize
Arimune(A
)[31]
27/M
NR
NR
NR
NR
NR
Unilateral
Taste
disturbance
NA
NR
NA
NR
Koya
ma
etal.(A
)[32]
20/M
NR
NR
NR
Yes
NR
NR
Tasteloss
24h
NR
6months
Malposition
Gaylard
[33]
40/M
NR
460
Yes
20ml
Unilateral
Numbness,
taste
disturbance
24h
Conservative
2months
NR
Majumderand
Hopkins[34]
27/F
NR
320
Yes
20ml
Bilateral
Numbness,
taste
disturbance
PACU
Conservative
6weeks
Nerve
compression
Ostergaard
etal.(A
)[35]
73/M
NR
NR
140
Yes
NR
NR
Taste
disturbance
1week
NR
6months?
partial
NR
Ahmedand
Yentis[36]
26/M
NR
430
Yes
30ml
Unilateral
Numbness,
taste
disturbance
PACU
NR
NR
NR
Laxton[37]
42/F
54
335
Yes
20ml
Unilateral
Numbness,
taste
disturbance
Few
hours
Conservative
4months
(90%
reco
very)
Multiple
factors
350 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
Table
2(continu
ed)
Reference
Age;
years/
sex
Weight;
kg
Size
Duration
of
surgery;
min
N2O
use
Cuff
pressure/
volume
measu
red
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
Pro-Seal
Brimaco
mbe
etal.[38]
61/M
74
5150
Yes
20ml
Unilateral
Numbness,
taste
disturbance
Immediate
Conservative
15days
Non-supine,
shoulder
surgery,
N2O,long
duration
Brimaco
mbe
andKeller[39]
64/F
76
445
No
2ml
Unilateral
Numbness
2h
Conservative
10h
Big
size
SupremeLM
AThiruve
nkatarajan
etal.[40]
45/F
61
3105
No
No
Tonguetip
Numbness
PACU
Conservative
3weeks
Smallsize
,cu
ffpressure
not
monitored
Rujirojindakul
etal.[41]
43/F
65
475
No
No
Tonguetip
Numbness
24h
Conservative
2weeks
Excess
cuff
pressure
i-gel
Renesetal.[42]
69/M
78
445
NR
NR
Bilateral
Numbness,
taste
disturbance
Few
hours
Conservative
8weeks
i-geldesign
Rujirojindakul
etal.[41]
33/F
53
345
No
NR
Tonguetip
Numbness
24h
Conservative
2weeks
NR
COPA
Kadry
and
Popat[43]
29/F
60
10
65
Yes
40ml
Unilateral
Numbness,
taste
disturbance
PACU
Conservative
10days
Multiple
factors
Laffon
etal.[44]
32/F
65
920
Yes
38ml
Bilateral
Numbness
PACU
Conservative
2h
Cuff
ove
rinflation
Inferior
alveolarnerve
Classic
LMA
variants
Hanumanthiah
etal.[45]
35/M
85
4120
Yes
30ml
Unilateral
Lowerlip
numbness
PACU
Conservative
2weeks
Vascular
compression
i-gel
Theronand
Loyd
en[46]
NR/F
NR
460
NR
NR
NR
Lowerlip
numbness
andulcer
NR
Conservative
4days
(partial)
i-geldesign
© 2014 The Association of Anaesthetists of Great Britain and Ireland 351
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
procedures [27]. However, although lingual nerve
damage does not lead to severe morbidity, disturbances
in taste, speech and the tongue trauma can cause sig-
nificant discomfort until recovery occurs.
The inferior alveolar nerve lies superficially between
the third molar tooth and the ramus of the mandible,
where it is vulnerable to injury [45] (Fig. 2). Injury pre-
sents as sensory loss of the lower lip resulting from
neuropraxia of the terminal branch (the mental nerve);
this creates the potential for subsequent lip trauma.
Both reported cases (cLMA and i-gel) recovered within
a week. The wide buccal stabiliser and the integral bite
block design of the i-gel makes it bulkier and harder
around the lips compared with other devices. This
could obscure the anaesthetist’s view of the lower lip
looking from the head end of the patient; accidental
taping of the lower lip to the lower bite block of the
i-gel might also contribute to nerve injury [46].
The only reported case of infra-orbital nerve injury
occurred with the LMA Supreme [25]. The maxillary
nerve continues as the infra-orbital nerve and inner-
vates the lower eyelid, upper lip, cheek and side of the
nose (Fig. 2). Injury to the infra-orbital nerve presents
as swelling and sensory loss of the upper lip. In the
report, the fixation tab of the device was fixed in close
contact with the upper lip [25]. The fixation tab is a
new feature, absent from other models of supraglottic
airway devices; it is a rectangular structure projecting
over the upper lip facilitating insertion and fixation.
According to the instructions from the manufacturer,
the distance between the fixation tab and upper lipTable
2(continu
ed)
Reference
Age;
years/
sex
Weight;
kg
Size
Duration
of
surgery;
min
N2O
use
Cuff
pressure/
volume
measu
red
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
infra-orbitalnerve
SupremeLM
ACarron
etal.[25]
64/F
68
480
No
60cm
H2O
NR
Numbness,
swelling,
(midline
upperlip)
PACU
Conservative
14days
Reduced
fixa
tion
tabto
lip
distance
COPA,cuffed
orop
haryngealairw
ay;NR,no
trecorded;PACU;po
st-anaesthesia
care
unit;A,abstract
data;EBUS,
endo
bron
chialultrasou
nd;TMJ,Tem
poromandibu
lar
joint.
Third molar
Lingual plate
Lingual nerve
Figure 4 Illustration of the lingual nerve entering themouth at the level of the 3rd molar tooth on the lin-gual side of the mandible, where it is close to the peri-osteum and prone to compression.
352 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
should be between 0.5 and 2 cm [50]. If the fixation
tab is found to press against the upper lip, a larger size
is warranted. The authors felt that this injury could
have been avoided by following the manufacturer’s
instructions. However, it may be difficult to maintain
this distance intra-operatively as the tape or tie secur-
ing the device is passed across the fixation tab, making
it difficult to inspect the distance. In addition, changes
in cuff pressure during anaesthesia may alter this dis-
tance [25].
Hypoglossal nerve injuryOur review identified 11 cases of hypoglossal nerve
injury [29, 51–60]. Of these, nine were after the cLMA
and two with the Pro-Seal (Table 3). Nine were isolated
injuries, the other two were bilateral. Eight cases were
reported in adults, two in adolescents and one in an
infant. Nitrous oxide was used in five patients and the
data were missing in three reports.
The hypoglossal nerve lies above the greater horn
of the hyoid bone at the angle of mandible before
turning forwards and medially towards the tongue
[51]. The nerve is vulnerable to neuropraxia from
compression injury due to an overinflated or malposi-
tioned cuff at the level of the greater horn of the hyoid
bone [61] (Fig. 2).
The nerve supplies the ipsilateral intrinsic and
extrinsic muscles of the tongue apart from the palato-
glossus [52, 62]. Ipsilateral injury presents as tongue
deviation to the affected side together with unilateral
muscle weakness [53, 63]. Bilateral injury manifests as
fasciculations, motor weakness of the tongue, dysar-
thria and dysphagia [54]. The onset time varied from
soon after awakening to as late as first postoperative
day. However, diagnosis can be confused by the co-
existence of other cranial nerve injuries. A review of
hypoglossal nerve injury after tracheal intubation
revealed that a quarter of the patients also had ipsilat-
eral lingual nerve damage [62]. These two nerves lie
closely together at the lateral margin of the tongue
where they can be compressed [62]. One of the two
reports with a Pro-Seal also had features of lingual
nerve injury [60]. As opposed to lingual nerve injury,
where both the cuff and the shaft of the supraglottic
airway can create pressure points, hypoglossal nerve
stretching is only related to the cuff of the device.
Internal carotid artery dissection and central venous
catheterisation through the internal jugular vein are
other rare causes of hypoglossal nerve injury [62].
Patients with severe or bilateral symptoms should
be referred to a neurologist for further management
(peripheral vs central tongue palsy). Extracranial
Doppler, duplex sonography or MRI may be required
to differentiate device-induced injury from internal
carotid artery dissection [62]. Spontaneous recovery is
possible with conservative rehabilitative measures such
as diet modifications, steroids and speech therapy [62].
All the reported patients recovered completely within a
few days to months, except one case where residual
motor weakness of the tongue persisted [57].
Cuff pressure was recorded in only one case
whereas the volume was mentioned in seven cases. In
two cases, an incorrect size was thought to contribute
to the injury [51, 58, 61].
Other contributory factors outlined from the
reports were: use of nitrous oxide; presence of a hypo-
pharyngeal haematoma in an anticoagulated patient;
extreme head rotation along with prolonged duration;
coexistent rheumatoid arthritis; and cuff overinflation
and malposition (Tables 3 and 4).
Multiple cranial nerve injuriesThere were two cases of combined lingual and glosso-
pharyngeal nerve injuries [31, 44] and one report of a
combination of lingual, glossopharyngeal and hypo-
glossal nerve injuries [29]. Glossopharyngeal nerve
injury presents as taste and sensory disturbance to the
posterior third of the tongue, loss of the pharyngeal
reflex, dysphagia, and deviation of the uvula to the
opposite side [47]. Temporomandibular joint subluxa-
tion was thought to account for the combination of
these three nerve injuries [29].
There was one case of Tapia’s syndrome, which is a
combined extracranial ipsilateral injury of the recurrent
laryngeal and hypoglossal nerves [8]. Pressure neuropr-
axia of both nerves due to an overinflated cuff and
stretching are the proposed mechanisms. The hypoglos-
sal nerve is situated on the most lateral prominence of
the transverse process of the first cervical vertebra and
crosses the vagus nerve [8]; the nerves are likely to be
stretched over this prominence. The patient described
also had features of lingual nerve injury [8].
© 2014 The Association of Anaesthetists of Great Britain and Ireland 353
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
Table
3Summaryof
hypo
glossalnerveinjuries
followinguseof
differenttypesof
supraglottic
airw
aydevices.
Reference
Age;
years/
sex
Weight;
kg
Size
Duration
ofsurgery;
min
N2O
Use
Cuff
pressure/
volume
measured
Laterality
Symptoms/
signs
Tim
eof
onset
Management
Tim
eto
reco
very
Contributing
factors
Classic
LMA
variants
Trujilloetal.[55]
9M/M
9.7
1.5
45
No
NR
Unilateral
Tongue
deviation
2h
Conservative
,speech
therapy
3weeks
NR
Fidelerand
Schroeder[29]
32/F
NR
460
NR
50cm
H2O
Unilateral
Tongue
deviation
Few
hours
Conservative
4days
TMJ
subluxa
tion
hyp
othesised
Lo[51]
48/M
NR
3120
NR
20ml
Unilateral
Tongue
deviation,
dysphagia
3h
Conservative
2weeks
NR
Rodriguezetal.[53]
15/M
NR
4NR
NR
NR
Unilateral
Dysarthria,
tongue
deviation
2h
Steroids
MRI
15days
NR
Sommeretal.[52]
15/M
88
490
No
20ml
Bilateral
Dysphagia,
dysarthria,
tongue
fasciculations
&motor
weakness
Immed-
iate
Steroids
MRI
4weeks
Extremehead
rotation,
prolonged
surgery
Stewart
and
Lindsay[54]
54/M
83
545min
Yes
40ml
Bilateral
Dysphagia,
dysarthria,
tongue
weakness,
7kgweight
loss
Immed-
iate
CNSco
nsult
Speech
therapy
6weeks
Cuff
ove
rinflation,
malposition
Umapathyetal.[56]
46/M
NR
4NR
No
NR
Unilateral
Tongue
deviation,
dysphagia
6h
Conservative
6weeks
NR
KingandStreet[57]
55/M
NR
4NR
Yes
25ml
Unilateral
Dysphagia,
dysarthria
4h
Conservative
8days
Antico
agulation
Nagaietal.[58]
62/F
36
33h
Yes
20ml
Unilateral
Dysphagia,
tongue
deviation
3h
Vitamin
B12,
steroids
1week
NR
Pro-Seal
Trive
di[59]
24/M
62
4300
Yes
30ml
Unilateral
Dysphagia,
dysarthria
1h
Steroids,
vitamin
B12
6weeks
Non-neutral
headposition,
N2O,
prolonged
duration
Tr€ umpelm
annand
Cook[60]
28/F
NR
5210
Yes
40ml
Unilateral
Dysphagia,
tongue
numbness
1day
Conservative
4months
N2O,prolonged
surgery
NR,no
trecorded;TMJ,tempo
romandibu
larjoint;MRI,magneticresonanceim
aging;
CNS,
centralnervou
ssystem
.
354 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
DiscussionInjuries to cranial nerves from supraglottic airway
devices present in different ways. In the reports we
retrieved, symptoms were minimal with trigeminal and
hypoglossal nerve neuropraxia, and the outcome was
good. Conversely, most patients with recurrent laryn-
geal injury presented with significant dysfunction.
Injuries can be complex in that, while many causative
mechanisms have been proposed, many happened
apparently for no identifiable reason. Awareness of
these injuries and their presentation is crucial in subse-
quent management. In the postoperative setting, anal-
gesics and residual anaesthetic drugs might mask
symptoms and signs, leading anaesthetists to overlook
the problem.
Although information on contributing factors and/
or the mechanism of injury was missing in over half the
reports included, two factors are worthy of mention.
The first is intracuff pressure. Even at recommended
cuff volumes, intracuff pressure can exceed the recom-
mended values [64] and potentially exceed the critical
capillary perfusion pressure of the pharyngeal mucosa
[65, 66]. Nitrous oxide diffusion into the cuff can
increase the cuff volume up to 38% within 30 min and
up to 50% before the end of anaesthesia [67]. Further-
more, if the cuff is inflated to the maximal recom-
mended volume, the cuff pressure can double within
60 min [68]. The cuff pressure varies between individ-
ual patients for a given volume of air [1]. A recent study
shows that, even in the absence of nitrous oxide, the
cuff pressure of the LMA can exceed the recommended
level in about three quarters of the patients; cuff pres-
sure was frequently over 120 cmH2O [69]. Measuring
the cuff pressure, and keeping it below 60 cmH2O, has
been shown to reduce pharyngolaryngeal complications
by 70% [3]. However, apart from the manufacturers’
recommendation of a maximum cuff pressure of
60 cmH2O, there are no clinical guidelines endorsing
this particular value, so others may be better.
Second, the case reports suggest that components
other than the cuff can also cause nerve injury. These
include the shaft of the device compressing the lingual
nerve at the periosteum close to the third molar, and
the fixation tab of the LMA Supreme causing infra-
orbital nerve damage. It is interesting to speculate
whether differences in device design might influence
their propensity to cause nerve injury – do the wider
shaft and the more rigid material of the LMA Supreme
make it more likely to damage the lingual nerve injury
compared with the cLMA, for instance? Current
knowledge suggests that directly measured pressures
exerted on the oropharyngeal mucosa were very low
and similar among cLMA, LMA Supreme and i-gel
[70, 71], so one might assume that they have a compa-
rable safety profile in this respect.
As many anaesthetists are more aware of periph-
eral nerve damage during anaesthesia and surgery,
some comparative features are relevant.
Most cranial nerve injuries are identified within the
first 24 h after surgery whereas peripheral neuropathies
are usually identified after 48 h [72]. Anaesthetic factors
play a predominant role in the presentation of cranial
nerve injuries, whereas surgical and predisposing factors
have a greater role in causing peripheral nerve injuries
[73]. Most of the cranial nerve injuries (apart from some
recurrent laryngeal nerve injuries) are neuropraxic in
nature. Hypertension, smoking and diabetes are well-
recognised risk factors of peripheral nerve injury [74];
however, data on a similar risk factors for cranial nerve
injury are lacking, though it seems plausible that those
with pre-existing neuropathic disease might be more
vulnerable. Lastly, while electromyography is widely
used in the management of peripheral nerve injury [75],
its utility was not described in the reports of cranial
Table 4 Possible contributing factors to cranial nerveinjuries with supraglottic airway devices.
Anaesthesia-related factorsExcessive cuff inflation, > 60 cm H2OFailure to measure and adjust the cuff pressureInappropriate size selectionPeri-operative manipulation of the deviceNitrous oxide useMalpositioningTraumatic insertionPoor techniqueChemical neuronitis
Patient-related factorsDiabetes mellitusCollagen vascular disordersPeripheral vascular disorders
Surgery-related factorsLateral positionExtreme head rotationProne positionProlonged duration
© 2014 The Association of Anaesthetists of Great Britain and Ireland 355
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359
nerve injury after supraglottic airway use. Nonetheless,
electromyography was employed in the management of
hypoglossal nerve palsy as a complication of tracheal
intubation [76] implying its possible role as a diagnostic
tool in nerve palsy after supraglottic airway use.
If cranial nerve injury is suspected, details of the
timing and progression of the symptoms, with a par-
ticular emphasis on the predisposing factors should be
elicited [75]. Attempts should be made to ascertain the
mechanism of injury and a basic neurological exami-
nation should be undertaken, concentrating on the
sensory and motor deficits. Simple assessments such as
light touch, pinprick and two-point discrimination
should be used to record baseline function and help
monitor progression. Documentation should include
schematic illustration of the areas involved, and the
nature of the injury should be well described. Patients
with minor neuropraxic injuries should be reassured
about recovery and followed up by telephone. Appro-
priate consultations should be organised as early as
possible for complicated presentations, including neu-
ropathic pain.
Although we systematically sought case reports
and series for this review, we did not include data
about cranial nerve injuries that might have appeared
within observational or randomly assigned studies of
supraglottic ariways. We did not contact device manu-
facturers nor national registries of medical device
problems. We are unable to calculate estimates of fre-
quency as the true number of nerve injuries is
unknown and we have no reliable denominator. Fur-
thermore, the evidence for specific causative factors is
moderate at best. Nevertheless, we have compiled the
largest collection of published reports to date and we
are in a position to make two comments for practice.
The first relates to device size. Currently, most
manufacturers recommend weight-based selection of
size of supraglottic airway device. However, Asai and
Brimacombe argue against using a single factor in size
selection, since there is no definite relationship
between gender, weight, height, dimensions of the oro-
pharynx and body mass index [77]. Individual ana-
tomical variations in relation to the shape and size of
the oropharynx are relevant when choosing a size of
LMA. A larger size mask where the cuff is not visible
in the back of the mouth and the cuff volume inflated
to the minimum necessary seems to be an appropriate
technique [77].
The second relates to causation. We suggest that
cranial nerve injuries may not be completely pre-
ventable and should not always be assumed to rep-
resent sub-standard care. Nevertheless, we advocate
the use of a cuff manometer and recommend that
the cuff pressure is maintained below < 60 cm H2O.
A careful, gentle insertion technique; proper fixation;
and early identification and correction of misplace-
ment will also help.
In terms of research, large prospective epidemio-
logical studies are needed to determine the true inci-
dence of these injuries, as well as improving our
understanding of them. A better knowledge of the ana-
tomical configuration of new devices might also con-
tribute to greater safety, and nerve injury should be
incorporated as a secondary adverse outcome in future
studies evaluating supraglottic airway devices. The dif-
ferences between various devices in causing these inju-
ries are also worthy of further investigation.
AcknowledgementsThe authors thank Dr Michael Draper, research librar-
ian at Barr Smith Library, University of Adelaide, for
his help in the literature search. We would like to
thank Mr Tavik Morgenstern, School of Medical Sci-
ences, University of Adelaide, Australia, for sketching
the diagrams depicted in this manuscript. We also
thank Dr John Currie, senior visiting anaesthetist of
our hospital for his valuable guidance and inputs in
preparing the revision.
Competing interestsNo external funding and no competing interests
declared.
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Appendix Details of the searchstrategy
PubMed(Laryngeal mask*[tw] OR Supraglottic airway*[tw] OR
Extraglottic airway* [tw] OR Supra glottic airway*[tw]
OR Extra glottic airway* [tw] OR Ultra CPV[tw] OR
Ultra clear CPV[tw] OR Ultraflex CPV[tw] OR Aura-
straight[tw] OR Auraonce[tw] OR Aura40[tw] OR
Auraflex[tw] OR Vital seal[tw] OR King LAD[tw] OR
King LAD flexible[tw] OR LMA Classic[tw] OR LMA
unique[tw] OR LMA flexible[tw] OR Cobra PLA perila-
ryngeal airway*[tw] OR Cobra Plus[tw] OR Portex soft
seal[tw] OR SLIPA[tw] OR Streamlined liner*[tw] OR i-
gel[tw] OR LMA-prosea[tw] OR LMA-Supreme[tw] OR
King/VBM LT/Lt-D[tw] OR King/VBM LTS-D[tw] OR
VBM LTS II[tw] OR VBM GLT*[tw] OR Esophageal
tracheal tube[tw] OR Rusch Easy Tube[tw] OR Aura-i
[tw] OR Air-Q/ILA[tw] OR LMA Fastrach[tw] OR
LMA classic excel[tw] OR Baska Mask[tw] OR Guardian
358 © 2014 The Association of Anaesthetists of Great Britain and Ireland
Anaesthesia 2015, 70, 344–359 Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices
CPV[tw]) AND (Cranial nerves[mh] OR Cranial nerve*
[tw] OR Lingual nerve*[tw] OR Inferior Alveolar
Nerve* [tw] OR Hypoglossal Nerve* [tw] OR Recurrent
Laryngeal Nerve* [tw] OR inferior Laryngeal Nerve*
[tw] OR Glossopharyngeal Nerve* [tw] OR Mental
nerve*[tw] OR Infra-orbital nerve*[tw] OR Infra-orbital
nerve*[tw] OR Cranial nerve injuries[mh] OR Cranial
neuropath*[tw] OR cranial neuropraxia*[tw] OR cra-
nial nerve neuropraxia* [tw] OR sensory loss*[tw] OR
tongue numbness*[tw] OR dysgeusia*[tw] OR taste*
[tw] OR Parageusia*[tw] OR Ageusia*[tw] OR Gusta-
tion [tw] OR Lip numbness[tw] OR Lip swelling[tw] OR
Swollen lip*[tw] OR Dysphagia*[tw] OR Deglutition
Disorder*[tw] OR Swallowing disorder*[tw] OR Dys-
arth*[tw] OR Tongue immobilit*[tw] OR Hoarseness
[tw] OR Stridor[tw] OR Respiratory Aspiration of Gas-
tric Contents[tw] OR Tracheostom*[tw] OR Vocal Cord
Paralys*[tw] OR Vocal cord Pals*[tw] OR Vocal fold
Pals*[tw] OR vocal cord pares*[tw] OR Vocal cord de-
formit*[tw] OR Laryngeal Paralys*[tw] OR Laryngeal
edema*[tw] OR Laryngeal oedema*[tw] OR Dysphonia
[tw] OR Phonation disorder*[tw] OR (lip[tw] AND
scabbing [tw])) AND (Case series [tw] OR Case report*
[tw] OR Case stud*[tw] OR Case histor*[tw])
Embase‘Laryngeal mask’/syn ORsupraglottic next/1 airway*
OR supraglottic next/1 device* OR extraglottic next/1
airway* OR extraglottic next/1 device* OR ‘supra
glottic’ next/1 airway* OR ‘Supra glottic’ next/1
device* OR ‘extra glottic’ next/1 airway* OR ‘extra
glottic’ next/1 device* OR ‘Ultra CPV’ OR ‘Ultra clear
CPV’ OR ‘Ultraflex CPV’ OR Aurastraight OR Au-
raonce OR Aura40 OR Auraflex OR’Vital seal’ OR
‘King LAD’ OR ‘LMA Classic’ OR ‘LMA unique’ OR
‘LMA flexible’ OR ‘Cobra PLA’ OR ‘perilaryngeal air-
way’ OR ‘Cobra Plus ‘ OR ‘Portex soft seal’ OR SLI-
PA OR ‘Streamlined liner of the pharynx airway’ OR
‘i-gel’ OR ‘LMA-proseal’ OR ‘LMA-Supreme’ OR
‘King VBM LT Lt-D’ OR ‘King VBM LTS-D’
OR’VBM LTS II’ OR ‘VBM GLT’ OR ‘gastrolaryngeal
tube’ OR ‘Esophageal tracheal tube’ OR ‘Rusch Easy
Tube’ OR ‘Aura-i’ OR ‘Air-Q ILA’ OR ‘LMA Fast-
rach’ OR ‘LMA classic excel’ OR ‘Baska Mask’ OR
‘Guardian CPV’ AND ‘Cranial nerve’/syn OR ‘glosso-
pharyngeal nerve’/syn OR ‘hypoglossal nerve’/syn OR
‘lingual nerve’/syn OR ‘mandibular nerve’/syn OR ‘max-
illary nerve’/syn OR ‘trigeminal nerve’/syn OR ‘vagus
nerve’/syn OR ‘Inferior Alveolar Nerve’/syn OR
‘recurrent laryngeal Nerve’/syn OR ‘inferior laryngeal’
next/1 nerve* OR mental next/1 nerve* OR ‘mental
nerve’/syn OR ‘infra-orbital nerve’/syn OR ‘infra orbi-
tal’ next/1 nerve* OR ‘infra-orbital nerves’ OR ‘cranial
nerve injury’/syn OR ‘glossopharyngeal nerve injury’/
syn OR ‘hypoglossal nerve injury’/syn OR ‘trigeminal
nerve injury’/syn OR ‘vagus nerve injury’/syn OR Cra-
nial next/1 neuropath* OR cranial next/1 neuroprax-
ia* OR sensory next/1 loss* OR tongue next/1
numbness* OR dysgeusia* OR taste/syn OR ageusia/
syn OR Parageusia* OR lip next/1 numbness* OR lip
next/1 swelling* OR swollen next/1 lip* OR dyspha-
gia/syn OR dysarthria/syn OR Tongue next/1 immobi-
lit*Hoarseness OR Stridor OR ‘Respiratory Aspiration
of Gastric Contents’ OR Tracheostom* OR ‘Vocal
Cord Paralysis’/syn OR ‘Vocal cord Palsies’ OR ‘Vocal
cord’next/1 deformit* OR Laryngeal next/1 (Paralys*
OR edema* OR oedema*) OR Dysphonia/syn OR
Phonation next/1 disorder* OR (lip AND scabbing)
AND (‘Case study’/syn OR ‘Case report’ OR Case
next/1 histor*)
© 2014 The Association of Anaesthetists of Great Britain and Ireland 359
Thiruvenkatarajan et al. | Cranial nerve injuries with supraglottic airway devices Anaesthesia 2015, 70, 344–359