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Spontaneous activity may be related to specific surgical maneuvers and should prompt
careful consideration of technique. Stretching
or clamping of the nerve, in addition to the
effects of cautery adjacent to the nerve, may
result in trains of spontaneous EMG response
that should resolve with cessation of the responsible maneuver [8]. Multiple studies, including
those of the senior author, have demonstrated
the safety of repetitive stimulations using constant current, pulsed stimulation in the 1–2 mA
range [10–13].
Advantages of Nerve
Monitoring
Some studies have determined that routine
identification of the RLN is associated with
lower rates of injury [8]. Monitoring may reduce
the incidence of intraoperative nerve injury,
and yet, it is not used universally [14]. Nerve
monitoring is a logical extension of anatomic
nerve visualization. We feel RLN monitoring
represents a very useful technical development
that may greatly aid the surgeon in identifying
and protecting the RLN during surgery in this
area, especially in difficult cases,e.g., large goiter,
inflammatory disease, extensive malignancy, or
reoperative cases. RLN monitoring adds a new
functional dynamic to thyroid surgery and adds
to visual information RLN monitoring can be
considered in has three modes: (1) to facilitate
neural identification, (2) to aid in neural dissection, and (3) to prognosticate regarding postoperative neural function.
Improved RLN Identification
and Dissection
First, for initial nerve localization before definitive identification, the blunt-tipped stimulus
probe may be used at higher intensity (e.g.,
2 mA) to probe and ‘‘neutrally map’’ the soft
tissue of the RLN triangle starting at a more
superficial level proceeding more deeply. This
technique often expedites identification of the
proximal portion of the RLN through targeted
dissection. In addition, once the RLN is identified, dissection of the nerve can be facilitated
especially through difficult surgical fields (such
as in a reoperative or radiated field or along
Berry’s ligament in cases of thyroiditis) through
intermittent test stimulation before division of
soft tissue structures adjacent to the RLN. Song
points out that monitoring can detect neural
discharge during retraction and may help prevent neuropraxic traction injury [15]. Monitoring can also signal return of function after a
traction injury. Thomusch et al. prospectively
studied over 4000 patients undergoing thyroidectomy with and without nerve monitoring. In
their study, patients who underwent surgery
with intraoperative RLN monitoring had lower
rates of both temporary and permanent RLN
injury (1.4 and 0.4%) compared with patients
having surgery without monitoring (2.1 and
0.8%) [16].
Prognostic Function
It is well known that the surgeon’s eye is not
reliable in predicting injury to the RLN in thyroid
surgery [17–19]. This leadsto an underestimation
of RLN injuries. Caldarelli has found that injury
to the RLN may be caused by stretch/traction,
pressure, crush, electrical injury, ischemia, and
suction injury in addition to transection [8]. The
bulk of nontransection injuries are hard to predict intraoperatively by visual assessment alone.
If ispsilateral RLN injury goes unrecongnized, the
patient is at increased risk if bilateral dissection is
planned. Empiric recommendations have been
made to perform prophylactic tracheotomy in
‘‘high-risk patients’’ and in ‘‘extensive resections’’
[20, 21]. Nerve monitoring can help provide
information to stage complex surgery and avoid
bilateral RLN injury and possible tracheotomy .
The study of intraoperative neural prognosticating for the RLN is based in part on substantial
experience with neural monitoring for predicting
injury to the facial nerve in cerebellopontine
angle surgery. These studies have suggested that
elevation in stimulation threshold after surgical
manipulation was related to postoperative deficit.
In analyzing data from over 1400 human cases as
well as those from a canine model of RLN injury,
the senior author has observed that in nontransection injuries to the RLN that result in postoperative vocal fold immobility, a decrease in
amplitude of the evoked response is seen with
less significant changes in latency and stimulation
threshold [8]. This wouldsuggest thatsome fibers
are intact to conduct the signal, but that a significant number have been injured resulting is lower
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MANAGEMENT OF THE LARYNGEAL NERVES AND VOICE
amplitude. However, studies by Eisele have
suggested that changes in stimulation threshold
after thyroidectomy correlate with postoperative
deficits in function. Increases in threshold by as
little as 0.1 mA have led to postoperative deficit.
The greater the threshold shift, the longer the
deficit can be expected. [22] Thomusch et al.
also analyzed the reliability of monitoring for
predicting RLN dysfunction in 15,403 nerves at
risk. They found that an intact stimulation signal
was 99.6% accurate in predicting normal postoperative nerve function. This can provide useful
information and reassurance for the patient and
the surgeon. [23]
The senior author has developed criteria that,
when present, accurately predict normal neural
function postoperatively. Study of intraoperative
EMG data from125 patients with normal postoperative RLN function has provided EMG
criteria that will predict normal postoperative
laryngeal function when present. These are
(1) initial setup criteria which confirm that the
nerve has been identified and that the monitoring
system is functioning properly and (2) final EMG
readings that predict normal postoperative
function [8]. If these are met, it should result in
complete avoidance of the complication of
bilateral vocal cord paralysis, even in cases of
transient injuries. If the first criterion is not met,
then the surgeon must check the system connections or consider the possibility that he has not
found the nerve. If the initial criteria are met but
the final EMG criteria are not, thena neural injury
is possible. The surgeon should first check for
laryngeal twitch. If present, then neural injury
has not occurred and the tube is likely malpositioned. If the twitch is not present, then one
should consider the following: (1) problem with
current delivery, (2) displacement of ground electrodes, (3) connection problem at connector box,
(4) stimulator probe malfunction, (5) neuromuscular blockade, (6) and finally neural injury [8].
Any correctable problems should be sought,
e.g., suture impingement on the nerve. However,
postoperative paralysis should be expected and
the surgeon must consider postponement of the
contralateral procedure. There are cases which
are associated with higher rates for RLN paralysis
for which monitoring is especially helpful
(Table 14.2). It is of note, however, that not all
difficult cases can be identified preoperatively.
Familiarity with the equipment is also improved
through routine application.
Monitoring the External Branch
Rates of injury to the EBSLN are between 9 and
14% [8]. Some authors recommend the use of
EBSLN monitoring viacricothyroid muscle needle
electrode in ‘‘high-risk’’ cases. We feel that the thin
cricothyroid muscle would be easily disrupted by
needle placement. We favor EBSLN stimulation
with visible detection of cricothyroid muscle
twitch. It is of note that EBSLN stimulation will
give a discrete tracing on the EMG endotracheal
monitor (amplitude half that of ipsilateral RLN
stimulation with very short latency) due to the
EBSLN’s extension, the human communicating
nerve [8].
In summary, nerve monitoring may assist
the surgeon with more rapid and confident
identification of the RLN and EBSLN during
thyroid and parathyroid surgery. It will also
facilitate dissection along the RLN which is
Table 14.2. Cases that may benefit from recurrent laryngeal nerve (RLN) monitoring[8]
1. Cases known to be associated with increased difficult dissection and risk of RLN paralysis:
a. Thyroid cancer
b. Significant lymph node resection
c. Graves’ disease/thyroiditis
d. Large cervical or substernal goiters
e. Revision surgery
f. Surgery after external-beam radiation therapy
2. Surgery on an only functioning nerve
3. Strong consideration for all cases:
a. Many difficult cases cannot be predicted based on preoperative data (e.g., nonrecurrent RLN)
b. Any bilateral case. Prognostic testing on first side allows safe, contralateral surgery without bilateral vocal cord paralysis
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especially useful in certain cases such as a
distally branching RLN or in cases of adhesive
ligamentous attachments (Berry’s ligament). As
discussed, it may be used to prognosticate
postoperative function and impact the decision
to perform bilateral surgery. When using endotracheally based systems, attention to detail
and confirmation of tube position preoperatively is essential. It must always be remembered that the monitor is not a substitute for
careful surgical technique and meticulous
hemostasis.
Surgical Maneuvers to Avoid Injury
to EBSLN
This delicate neural structure travels just lateral to the thyroid cartilage on or just under
the lateral surface of the inferior constrictor
muscle in the cricothyroid space. Aggressive
retraction or cautery near the superior pole in
the cricothyroid space may lead to injury. The
cricothyroid muscle can also be injured directly
through aggressive dissection or cautery on the
anterolateral cricoid region. The EBSLN may be
entrapped during dissection of the superior pole.
En-masse division of the superior pedicle may
lead to transection. We favor individual dissection and division of superior vessels from medial
to lateral direction with careful inspection and
electric stimulation with cricothyroid muscle
observation. Injury results in lack of vocal range
and possible changes in pitch as noted above.
Exceptional care must be taken to avoid these
mistakes.
The EBSLN has significant anatomic variation, and for this reason, some have suggested
that the nerve must be visualized in order to
prevent surgical injury [2, 24]. We agree that
routine identification as a simple and expeditious maneuver that may decrease the incidence
of injury significantly [24].
Intraoperative Injury to the SLN
By far the best means of dealing with intraoperative SLN injury is by identification and
avoidance as currently, to our knowledge,
there have been no reports of neurorrhaphy or
reinnervation. Early speech rehabilitation is to
be employed in symptomatic patients [25]. This
is perhaps the only mode of therapy.
Surgical Maneuvers to Avoid Injury
to RLN
Neural injuries to the RLN may be partial or
complete and may be temporary or permanent.
The RLN may be injured by multiple mechanisms which in turn relate to either patient disease or to iatrogenic injury. Benign processes
such as thyroiditis (Graves’, Hashimoto’s, and
Riedel’s viral thyroiditis), the solitary nodule,
multinodular goiter, parathyroid adenoma,
and substernal goiter may surround and or
infiltrate the nerve with or without paralysis.
The incidence of vocal fold paralysis in patients
with benign thyroid disease is approximately
1% or less [26, 27]. Studies have also shown
that 38–89% of these cases of paralysis will
recover following surgery and that recovery is
more likely in cases of paralysis of shorter duration [26]. It is worth noting that in these cases of
gradual growth, there is often no symptomatology as the opposite vocal fold may compensate
slowly to obscure any clinical manifestations.
There have been many studies of involvement
of the RLN by malignant tumors. The overall
incidence of local invasion with papillary cancer
is 16% with the RLN being the second most
common site of invasion after strap muscle
invasion [28, 29]. Falk and McCaffrey studied
262 patients with invasive well-differentiated
thyroidcarcinoma.Ofthese,123hadinvasionof
the RLN. They found no difference in survival
between patients who had their nerve resected
versus those who did not if postoperative radioiodine and suppressive T4 was employed. Most
patients failed distantly if they failed at all [30].
Most evidence suggests that a nerve that is
preoperatively paralyzed and infiltrated with
carcinoma will not recover function if preserved
at surgery. Given this fact, we feel it should be
sacrificed for oncologic benefit. RLN paralysis
from thyroid lymphoma may be an exception to
this generalization as nerve function may
return following nonsurgical treatment of lymphoma [30].
If the nerve is functional preoperatively but
found to be infiltrated at surgery, then every
attempt should be made to maintain its anatomic integrity unless it would lead to leaving
gross malignancy behind. It should be kept
in mind that radioiodine therapy and T4 suppression represent possible modalities for
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MANAGEMENT OF THE LARYNGEAL NERVES AND VOICE
treatment of residual microscopic disease. It is
clearly imperative for the surgeon to be aware
of the preoperative status of the vocal fold
before undertaking any surgery. This evaluation is accomplished by preoperative indirect
laryngoscopy.
Routine Identification
As stated above, modern studies have agreed
that routine identification of the RLN during
thyroid surgery will result in a lower incidence
of nerve injury and associated voice changes.
Therefore, it is advisable to definitively identify
the nerve in every case. Various approaches
exist to do this.
Most commonly, thenerve is identified in the
recurrent triangle after limited lateral dissection
of the thyroid lobe. It is located between the
common carotid artery and the trachea, at a
level inferior and ventral to the inferior thyroid
artery. The nerve monitor may assist with this
as previously discussed through the above
described neural mapping technique. It can
then be dissected superiorly to its laryngeal
entry point, so that the ligamentous attachments of the thyroid lobe are divided with the
nerve in view. We favor this lateral approach for
routine first time surgery.
It may also be identified more inferiorly
before significant thyroid lobe dissection. This
approach is helpful with large goiters revision
cases and where a lateral approach is more difficult. Once found, the RLN is then dissected
superiorly to the laryngeal entry point. We especially favor this approach in revision cases
where scarring may prohibit the routine lateral
approach described above. Through this inferior approach, the revision surgeon may find the
nerve below the first surgeon’s scar.
In cases of goiter, whether cervical or with
significant retrosternal component, it may be
difficult if not impossible to identify the nerve
through the above described lateral or inferior
approaches. In these instances, it will be wise for
the surgeon to search for the nerve and begin
efforts to identify it at the superior pole through
the superior approach to the RLN. The superior
pole is carefully isolated with attention to the
EBSLN. Subsequently, the RLN may be identified superiorly near the laryngeal entry point.
The inferior cornu of the thyroid cartilage as
well as the lateral edge of the cricoid cartilage
are the landmarks of interest. Once identified
here, it may be traced proximally as the goiter is
dissected and removed (Fig. 14.4).
Nerve Injury
The pathophysiology of RLN injury, like other
peripheral neuropathy, may be considered to
range from neuropraxia (i.e., mild traction or
dissection injury) to full neurotmesis with complete fascicle-perineural disruption and subsequent Wallerian degeneration (i.e., transection
injury) as described by Sunderland [31].
Iatrogenic injury may have numerous causes
and consequences. Rates of iatrogenic injury
may vary widely (1–25%) and are not always
easy to interpret for a variety of reasons. RLN
injury may be underreported due to failure to
recognize injury on the part of the surgeon as
well as failure to perform routine postoperative
laryngeal exam.
It is important to understand that there are
many causes of postoperative voice change
without RLN or SLN injury. These non-neural
sources of postoperative voice change are
almost always temporary but often indistinguishable from neural injury by voice quality
alone. Laryngeal exam is essential in distinguishing amongst the various causes of postthyroidectomy voice change. We have proposed
the following system for organizing the causes
of postoperative voice change (Table 14.3).
Usually, postoperative dysphonia from
non-neural causes is temporary. Most cases
of long-term dysphonia, however, will be due
to iatrogenic nerve injury. The only way to
arrive at accurate estimates of overall true
rateofRLNinjuryistoassessallpatients
undergoing thyroidectomy both before and
after all surgery by indirect laryngeal exam
by one versed in laryngoscopy.
For these and other reasons, the true rate of
RLN injury must be discussed as temporary and
permanent injuries (those lasting more than
6–12 months). The rates of 1% that are quoted
in the literature may be biased by underreporting due to lack of laryngeal exam postoperatively. Also rates may vary with pathology and
with the particular procedure performed. Injury
to the RLN is more common in the following
situations: lack of identification at surgery,
bilateral surgery, surgery for cancer, surgery
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Fig. 14.4. Relationship of the recurrent laryngeal nerve and the thyroid gland. Techniques for nerve identification. (A) RLN is
identified inferiorly in the recurrent triangle. The inferior pole is reflected superiorly and inferior parathyroid gland is depicted in situ
in the thyrothymic horn. (B) RLN is identified superiorly near its laryngeal entry point. This technique can be helpful in revision cases
and with substernal goiter. (C) Lateral view of left thyroid lobe reflected medially. The RLN is seen in the tracheoesophageal groove
in close relation with Berry’s ligament. This figure was published in Surgery of the thyroid and parathyroid glands, Randolph GW, ed.
Copyright Elsevier 2003. Reprinted with permission.
associated with extensive lymph node dissection, surgery for Graves’ disease or thyroiditis,
revision surgery, surgery associated with substernal goiter, surgery with longer operating
times or greater blood loss, and patients
brought back for bleeding [8].
The effects of injury on the RLN on the
patient are not easy to predict. Temporary
lesions will likely result in complete recovery
with time. Permanent paralysis may present
with mild to severe dysphonia. However,
some patients have near normal speaking
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MANAGEMENT OF THE LARYNGEAL NERVES AND VOICE
Table 14.3. The causes of postoperative voice change
after thyroid surgery
1. RLN paralysis or paresis
2. SLN paralysis or paresis
3. Endotracheal associated:
a. Direct vocal cord injury or edema
b. Arytenoid dislocation
c. Paralysis
4. Regional non-neural effects:
a. Strap muscle injury or denervation
b. Global perilaryngeal neural plexus (nonmotor)
disruption
c. Global regional scar /fixation
d. Inflammatory change cricothyroid muscle
5. Coincident voice change unrelated to surgery, ex viral
neuritis
voices even with complete unilateral paralysis
(a reason for underreporting in some studies)
while others have significant vocal fatigue and
air escape leading to a breathy voice quality,
vocal fatigue, and poor projection. Other
symptoms include varying levels of dyspnea
and possible aspiration. Some patients will
present with coughing paroxysm due to
chronic aspiration of saliva and others with
frank aspiration pneumonia.
Traction Injury
Traction injury is a neuropraxic injury that will
often improve with time if the traction is
relieved. The nerve monitor allows the surgeon
to recognize this type of injury and to make
appropriate modifications in technique to
improve it. Spontaneous EMG activity is followed by a period of no response to stimulation
proximal to the injured site [8].
Crush Injury
Studies in dogs and observations in humans
have suggested that nontransection crush injuries need not be repaired and have a reasonable
prospect for recovery. In dogs, function may
recover in 4–8 weeks [8].
Suture Impingement
It is possible to entrap the RLN with a suture
ligation of vascular structures. Once again, this
type of injury may easily go unrecognized, but
may be revealed through nerve monitoring as it
will result in a decrease or cessation of electrical
response. The exact point of the injury can be
identified through ‘‘injury site mapping’’ of the
injured nerve. Stimulation of the RLN at a point
proximal to the suture will not result in
response whereas stimulation distal to the site
of injury will yield a normal EMG tracing [8].
This area can then be examined carefully and
the suture removed to provide the best chance
for return of normal function. Suture ligation
would not be expected to recover if not released.
Cautery Injury
The potential deleterious effects of thermal and
electrical energy on peripheral nerves is well
known. Monopolar cautery causes significant
injury to myelinated and unmyelinated peripheral nerves including marked damage to
Schwann cells [32]. We favor limited bipolar
cautery with a small fine-tipped bipolar instrument in the area of the ligament of berry, allowing time for the region treated to cool between
applications
Intraoperative Resection/
Transection
Before resecting a RLN, it should be remembered that radioiodine and T4 suppression is a
viable option in cases of residual microscopic
disease, and external beam radiation may play a
role in selected patients. In some cases of invasive malignancy, it will be necessary to resect a
segment of the RLN. The typical scenario for
RLN resection would be an immobile cord on
preoperative laryngoscopy and frank gross
invasion by malignancy found intraoperatively.
Options for repair would include primary anastomosis or reinnervation procedure. Primary
anastomosis employs interrupted 10-0 nylon in
the epineurium. Early studies of results after
neurorrhaphy by Horsely in 1909 and Leahy in
1929 reported normal postoperative function
[8]. More recent studies have recorded return
of EMG activity but poor functional results [33,
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ENDOCRINE SURGERY
34]. It appears that adductor function predominates after neurorrhaphy and that paradoxical
vocal fold motion can be seen due to misdirection of abductor and adductor fibers [35, 36].
These results may be expected given that
adducting fibers outnumber abductors in the
RLN and the majority of laryngeal musculature
serves an adducting function [37, 38]. On the
other hand, some authors believe outcome is
better with neurorrhaphy due to improved resting tone of the vocal fold and improved position
of the arytenoid cartilage [39].
In cases where primary anastomosis is not
possible, reinnervation may be preferable for
maintenance of thyroarytenoid muscular tone
and improved arytenoid position. Options
include reinnervation with ansa cervicalis,
phrenic nerve, and vagal nerve. The best option
is ansa cervicalis (sternothyroid branch) – RLN
anastomosis according to Crumley [40]. This
type of repair is ideal after segmental defect
from RLN resection in cases of malignant infiltration. This may be performed to the distal
main or adductor branch of the RLN with the
goal of achieving a medialized cord with sufficient bulk to prevent aspiration and to allow
apposition of the mucosal edges. There is minimal donor nerve morbidity with this procedure
compared with other donor nerves. This may be
combined with cord injection simultaneously or
with open thyroplasty/arytenoid adduction at a
later time. (see below) While these procedures
are not likely to restore normal functional
mobility to a transected nerve, they may provide
muscular tone to the vocal fold that may
enhance voice quality and potentially prevent
aspiration. It is recommended that this repair
be performed within 24 months following
injury [40].
There may be an occasion where the surgeon is faced with an intraoperative iatrogenic
transection injury. The options for management of transection include primary neurorrhaphy or cross innervations as described
above. In addition, injection thyroplasty may
be performed simultaneously with or in place
of an attempted neural repair. With this technique, an injection is made just lateral to the
vocal processof theaffected arytenoid cartilage
in order to medialize the immobile vocal cord.
Slight overinjection may be advantageous
as some resorption may be expected with
time. Of course, caution is advised to avoid
compromise of the airway. Various substances
have been used and most have temporary effect
which can last 3–6 months. Common substances
now include autologous fat, collagen, gelfoam,
and hydroxyl appetite [41–43]. Teflon had been
used in the past withmore durable effect, but was
associated with laryngeal granuloma that could
cause airway compromise and so has been largely abandoned [44].
Recovery
Overall, it has been shown that recovery can be
seen in up to 40% of patients sustaining vocal
cord immobility after thyroid surgery [8].
Recovery of vocal fold immobility may be
expected to occur over the first 6 months following injury in 80% of cases where it will recover
[45]. Recovery is more likely after surgery for
benign disease [46] and when the nerve was
identified [47]. Treatment may include steroids
for transient, mild RLN injury. Lore has found
that rates of temporary immobility are much
lower (9.1 versus 2.6%) with the use of perioperative steroids [48].
As discussed below, management of a
permanent RLN paralysis may challenge the
thyroid surgeon or laryngologist postoperatively. Vocal fold immobility that lasts more
than 6 months may be considered permanent.
These patients would temporarily benefit from
injection procedures mentioned above and
might potentially be considered for reinnervation. However, most laryngologists would likely
opt for a long-term but static medialization
procedure such as the open thyroplasty (Isshiki
thyroplasty). This is the state of the art static
procedure for paralytic dysphonia that involves
creating a window in the thyroid cartilage
and bolstering the true vocal fold in a medial
position to enhance cord apposition with the
contralateral mobile cord. This procedure had
been performed in the past with sculpted silicone shims [49, 50], but more recently has been
successfully completed with Gore-Tex implants
[51]. This procedure may be performed under
local or general anesthesia. If done under local
anesthesia, patient vocalization can help guide
the surgeon’s efforts. Arytenoid adduction can
be combined with medialization laryngoplasty
especially when the affected cord is lower than
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MANAGEMENT OF THE LARYNGEAL NERVES AND VOICE
the normal cord for optimum vocal strength
and range [52].
Voice Changes with Thyroid
and Parathyroid Surgery
Perhaps since the time of Kocher, who was
awarded the Nobel Prize in medicine for his
refinements in the technique of thyroid surgery, attention has been focused on the minimization of operative morbidity. The major
morbidity associated with thyroidectomy
remains paralytic dysphonia. While symptomatic presentation in these instances is often
clear, there are cases that are not so evident
despite complete vocal fold immobility. Even
more difficult are incomplete limitations
in cord movement. The resultant vocal
changes associated with these injuries are
not always simple to predict or even to accurately describe clinically. Close examination
in recent years has shown that the changes
resulting from RLN injury may be variable
and, in addition, other lesions can lead to
alterations in voice even in the absence of
RLN paralysis. It is only recently that we
have recourse to the advanced techniques of
laryngology and voice analysis that enable us
to record, study, correlate, and understand
the many vocal consequences of thyroid surgery (See Table 14.3).
Neural Injury
The presentation of RLN and EBSLN injury
has been discussed in more detail above. The
clinician may notice clues to underlying voice
problems prior to more formal evaluation by
noting the patient’s respiratory pattern and
speaking voice. Dyspnea and stridor in the
early postoperative period may be signs of bilateral vocal lesions while a ‘‘breathy’’ voice due to
air escape during phonation, vocal fatigue, and
lack of projection may indicate a unilateral RLN
injury. Limited vocal range and pitch can be a
reflection of SLN injury and malfunction of
the cricothyroid muscle and perhaps laryngeal
framework [53].
Non-Neural Laryngeal Injury
Like neural injuries, non-neural injuries may be
due to the extent of patient disease or may be
iatrogenic. Benign or malignant thyroid tumors
and associated inflammatory conditions may
affect the endolarynx as well as the laryngeal
skeleton and musculature in addition to the
laryngeal nerves. It is now believed that many
of the changes in the voice after thyroid surgery
arise from changes that are non-neural in
nature.
It has been shown that intubation alone may
affect the postoperative voice temporarily and
even permanently in very rare cases. Vocal cord
edema and posterior granuloma due to intubation trauma are relatively rare but recognized
risks of general anesthetic with intubation.
These may be responsible for temporary
changes in voice whereas injuries such as
arytenoid dislocation may cause permanent
dysphonia. Voice changes may be seen in 5%
of patients after intubation alone [54].
Some have suggested that it is a change in the
laryngeal mechanics created by a disruption of
the extralaryngeal framework (e.g., strap muscles) that is responsible for dysphonia. Hong
and Kim evaluated vocal function in 54 patients
and found that even in the absence of RLN or
EBSLN injury, patients experienced vocal fatigue as well as changes in the speaking and singing voice. Indeed, acoustic analysis revealed
changes in the speaking fundamental frequency,
range of speaking fundamental frequency, and
vocal range after surgery [55]. Soylu et al. prospectively studied 48 consecutive patients who
had undergone thyroidectomy without reported
nerve injury [56]. The acoustic voice analysis
was performed preoperatively, on the second
postoperative day, and 3 months after the
operation. All patients in the study had demonstrable deficits on the test battery. A significant
minority of patients (37.5%) complained of subjective voice changes in the early postoperative
period. Those who did not remained symptom
free throughout the study period. Only 14.6%
had symptom complaints that failed to resolve by
3 months and these patients demonstrated
changes in the mean vocal fundamental frequency
(F
) only. Lombardi prosepectively examined
0
39 patients for voice and swallowing changes following total thyroidectomy using techniques
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ENDOCRINE SURGERY
including video strobolaryngoscopy and acoustic
voice analysis preoperatively as well as at 1 week,
1 month, and 3 months postoperatively, and discovered in this patient population without any
nerve injuries, mild change in voice and swallowing were experienced by a majority of patients
after total thyroidectomy. While these changes
reached the level of statistical significance, most
had resolved by 3 months postoperatively [57].
Musholt and Musholt studied over 130 patients
undergoing thyroid and parathyroid surgery in a
prospective four-arm study of changes in the
speaking and singing voice postoperatively. They
found that in the more extended procedures, the
highest pitch of the singing voice decreased significantly, especially in women. Changes in speaking voice remained subclinical [58]. Although the
mechanism of postthyroidectomy voice disturbance in patients with preserved nerve function
is not yet fully understood, it appears to be temporary and may be attributed to surgical trauma,
laryngotracheal fixation of the prelaryngeal
strap muscles, or trauma to the arytenoids,
e.g., during intubation [56, 57]. As these injuries
are often more difficult to identify than neural
injuries and their mechanisms have yet to be completely elucidated, often little more than voice
rehabilitation with a speech pathologist is offered
as treatment.
Voice Evaluation
When there is concern on the part of the patient
or the surgeon that a pertinent dysphonia exists,
it must be evaluated in an objective manner.
There are a number of clinical tools that may
be used during this evaluation.
Laryngoscopy
As stated above, the larynx must be evaluated preoperatively and postoperatively in
order to accurately understand the effects of
thyroid disease and surgery upon the larynx.
The appearance of the larynx should be symmetrical at rest and in phonation. With vocal
cord paralysis, the vocal folds may not meet
in the midline upon volitional adduction,
and the affected cord will usually remain
lateralized in a paramedian or fully abducted
position. The true vocal fold often appears in
a bowed state and the arytenoid often will be
displaced anteriorly giving the cord a shortened appearance. Laryngoscopy has been
shown to be highly sensitive in diagnosing
vocal movement abnormalities due to RLN
injury [3].
Stroboscopy
Stroboscopy is a technique, often performed by a
voice specialist or laryngologist, that allows
observation of the anatomic and functional
(vibratory) behavior of the vocal cords in the
awake patient during a brief office procedure.
The mucosal wave is responsible for vocalization
and involves the three-dimensional movement of
the superficial epithelial layer of the vocal fold
over the deeper lamina propria [1]. The strobe
employs a flashing light at a frequency that is set
based upon, but varying slightly from, the
patient’s fundamental vocal frequency. This
allows examination of the mucosal wave through
its entire cycle rather than obtaining a repeating
snapshot of the same point in the phonatory
cycle. It has greatly enabled the laryngologist to
better understand, diagnose, and treat a variety
of vocal cord pathologies including partial and
complete vocal immobility.
Video stroboscopy may pick up the
mechanical defects in cord function associated with dysphonia and can confirm vocal
fold movement deficits when present. A
recent study has suggested that this test is
100% sensitive and specific in diagnosing
vocal fold abnormalities after thyroid surgery
[59]. However, this would not be a costeffective method for vocal evaluation for all
patients, especially when compared with
indirect laryngoscopy. Its utility would be
realized, however, in those symptomatic
patients manifesting with persistent clinical
evidence of dysphonia before and after
undergoing treatment.
Laryngeal Electromyography
Laryngeal electromyography (LEMG) is a
potentially objective means for the evaluation
of laryngeal function both before and after surgery. In this technique, electrodes are placed in
various laryngeal muscles (most commonly
thyroarytenoid, posterior cricoarytenoid, and
209
MANAGEMENT OF THE LARYNGEAL NERVES AND VOICE
cricothyroid) to detect depolarizations evoked
by neural stimulation. Three basic patterns
emerge, including normal, neuropathy, and
myopathy. This test can best differentiate
between nerve injury and other mechanical
causes of vocal fold dysfunction such as myopathy or fixation of the cricoarytenoid joint. It
may also help differentiate cases of partial from
complete paralysis. For example, in cases of
partial injuries, a pattern marked by decreased
amplitude of LEMG responses and delayed
latency of response is seen [60]. Decreased
evoked potentials, decreased recruitment,
longer latency, and lower amplitude responses
are frequently seen in neuropathic injuries. In
the most severe neuropathic injuries (transection), no spontaneous or evoked potentials are
observed and one sees fibrillation potentials and
sharp waves on LEMG and evoked LEMG [60].
While exact patterns may vary, it is generally
agreed that findings of decreased recruitment,
polyphasic waveform morphology, altered
motor unit action potential amplitude, spontaneous activity, and evidence of synkinesis are
reliable indicators of neuropathy [61]. The
reader is referred to an excellent review of the
technical aspects and clinical applications of
this electrophysiologic test [62].
Studies to determine if LEMG can be used to
prognosticate recovery postoperatively are
based upon electromyographic studies of facial
nerve injuries. Munin et al. evaluated a series of
31 patients who had symptomatic vocal cord
immobility and determined that LEMG could
correctly predict recovery of function in 66.7%
of patients who had a negative test (i.e., excellent prognosis). Positive LEMG results (i.e., fair
or poor prognosis) correctly predicted the failure of recovery in 80% of patients [63]. LEMG
results are most useful during the 6 months after
injury. Afterwards, they may be misleading [35,
64, 65]. Therefore, LEMG data may direct
intervention in the first 6 months, e.g., cases of
suspected transection with no response or
fibrillation by LEMG. Otherwise, it is the opinion of the senior author that intervention for
immobile vocal fold should be considered if no
signs of recovery are present at 6 months [8].
Action may be taken sooner in cases of definite
transection or in symptomatic patients, e.g.,
with aspiration or marked dyspnea.
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