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156
P. V. Pradeep
Editor’s Note
EBSLN palsy is underdiagnosed since the subtle symptoms are ignored by many
patients and surgeons too. But consequences are of great signicance in patients
whose profession demands absolutely normal laryngeal function. Early voice
fatigue, inability to raise pitch and decrease pitch exibility are some of major
effects which compel many to change their profession. Video-stroboscope may
reveal posterior rotation of paralysed side, bowing and inferior displacement of
vocal folds. Voice rehabilitation therapy is always indicated for restoration of normality. The objective of therapy includes strengthening of crico-thyroid muscle.
Post-thyroidectomy transient hypocalcaemia is experienced in about 19–38% of
patients and permanent hypocalcaemia is recorded up to 3% of patients. Permanent
hypocalcaemia has lasting effects on skin and skin appendages, eyes and cardiac
musculature. Postoperative calcium estimations at 6 and 12h showing a negative
slope is a rough indicator of impending hypocalcaemia. More accurate predictor is
estimation of serum PTH (10min to 24h post-thyroidectomy) but with questionable
specicity.
References
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manage them and observations of their possible effect on the whole patient. World J Surg.
2000;24:971–5.
2. Ozbas S, etal. Comparisons of the complications of subtotal, near total and total thyroidectomy in the surgical management of multinodular goiter. Endocr J. 2005;51:199–205.
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8. Pradeep PV, Ramalingam K, Jayashree B.Post total thyroidectomy hypocalcemia: a novel
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of the external branch of the superior laryngeal nerve. Head Neck. 1992;14:380–3.
13. Rosato L, etal. Complications of thyroid surgery: analysis of a multicentric studyon 14,934
patients operated on in Italy over 5 years. World J Surg. 2004;28:271–6.
11 Complications ofThyroid Surgery (Except Vocal Cord Palsy)
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16. Sosa JA, etal. The importance of surgeon experience for clinical and economic outcomes from
thyroidectomy. Ann Surg. 1998;228:320–30.
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1993;102:441–6.
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157
Management ofVocal Fold Palsy
inThyroid Surgery
JayakumarRMenon andManjuE.Issac
12.1 Introduction
The close anatomical relationship of both the recurrent laryngeal nerve (RLN) and
external branch of the superior laryngeal nerve (ExSLN) to the thyroid gland makes
it vulnerable to injury during thyroid surgery. Despite all development in the knowledge of anatomy, skills, and techniques and inclusion of intraoperative nerve monitoring (IONM), thyroid surgery remains number one among the iatrogenic causes
for recurrent laryngeal nerve injury! This chapter is an attempt to cover the presentation and management of vocal fold paralysis following thyroid surgery.
A vocal fold palsy following thyroid surgery is a result of a direct injury or traction on the nerve or a thermal injury from a cautery. Sometimes it is quite a surprise
to the experienced surgeon who is well sure about the integrity of the nerve. A temporary or permanent vocal fold paralysis following thyroid surgery varies from 0 to
5.8% [1]. It is noted that the risk of injury was increased in revision thyroid cases
for benign or malignant diseases equally. Most studies reveal that the complications
are more with malignant pathology, hyperthyroidism, thyroiditis, retrosternal goiter,
and Grave’s disease [2, 3].
12
12.2 Recurrent Laryngeal Nerve (RLN)
The RLN supplies motor input to all the intrinsic muscles of the larynx except the
cricothyroid and the sensory innervations to the glottis, sub-glottis, proximal trachea, and esophagus.
COURSE: The vagus nerve courses downward in the neck after exiting the
jugular foramen. The RLN axons congregate at the ventromedial aspect of the
J. R. Menon (*) · M. E. Issac
Dr. Jayajumar’s Laryngology Group, Thiruvananthapuram, Kerala, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2024
C. G. Nair, S. J. Abraham (eds.), Surgical Management of Thyroid and
Parathyroid Diseases, https://doi.org/10.1007/978-981-97-3774-1_12
159
160
J. R. Menon and M. E. Issac
vagus nerve before branching. It travels in the carotid sheath and on the right side
of the neck it passes over the subclavian artery and loops around it and travels
cephalad in the neck towards the larynx. In less than 1% of cases on the right
side, its branches directly from the vagus to the larynx at the level of the cricoid
cartilage, the non- recurrent laryngeal nerve. This is explained by abnormal
embryological development. Normally RLN is pulled caudad in the neck along
the sixth arch. The left sixth arch remains as ductus arteriosus and later the ligamentum arteriosum. The right sixth arch resorbs and the right RLN passes inferior to the right fourth arch which becomes the subclavian artery. In rare situations
where the right fourth arch also resorbs during embryonic development; the right
subclavian artery arises from the descending aorta and right RLN branches from
the vagus in the neck and enter the larynx directly without looping around a vascular structure. There are only a few reports of non-recurrent laryngeal nerve on
the left side.
RLN ascends towards the neck from lateral to medial and courses upwards in the
tracheoesophageal groove. The course of the nerve in the tracheoesophageal groove
is important because several studies show that the course is variable, and one such
variability is its anterolateral position where it poses a signicant risk for iatrogenic injury.
There is often a branch of the inferior thyroid artery which is in close anatomical
relationship with the anterior and posterior branches of RLN and can place the
nerve at signicant risk if one of these vessels bleed.
The retro-thyroid segment of RLN is also susceptible to surgical trauma. The
relation of nerve to the posterior suspensory ligament of Berry can be lateral, medial,
or through the ligament which is another site of injury. The Tubercle of Zuckerkandl
is found in 63% and is another site of injury in the retro-thyroid segment [4].
12.3 Nerve Injury andSynkinesis
Understanding the basic issues in a paralyzed larynx is important in taking the right
step regarding intervention. The loss of signal conduction due to demyelination
without disruption of axons is termed neuropraxia which is temporary. But in the
case of axonotmesis due to crush injury, there is disruption of axons and during
recovery regenerating axons enter the corresponding endoneurial tubes. In neurotmesis, the structure of the nerve is disrupted, and regenerating axons enter the endoneurial conduits which end up in the wrong muscle. This is synkinesis which leads
to the contraction of antagonistic muscles. As a result, there is no vocal fold movement during phonation or inspiration or for airway protection or the larynx exhibits
paradoxical movement. Neurotmesis is evident on re-exploration as neuroma formation and scarring of the nerve can be seen in stretch injury. Impaired vocal fold
motion due to synkinesis is a severe and major cause (66–88%) of all paralysis [5].
Loss of vocal fold motion can happen as a result of inadequate or dysfunctional
reinnervation or denervation. Since RLN carries both adductor abductor bers,
regeneration is more problematic.
12 Management ofVocal Fold Palsy inThyroid Surgery
161
12.4 Unilateral Vocal Fold Paralysis
A neuropathological study of unilateral vocal fold palsy at a tertiary care center
revealed that thyroidectomy continues to be the single most common surgical procedure responsible for unilateral vocal fold palsy [6]. The symptoms of unilateral
vocal fold palsy are related to glottis insufciency. Hoarseness of the voice in the
immediate post-operative period needs attention to have a look at the movement of
vocal folds with a beroptic laryngoscope. The voice quality varies from mild
hoarseness in a compensated case to severe aphonia. Some patients develop swallowing difculties such as cough on taking food especially liquids. They will have
a weak and inefcient cough. Some patients may complain of being short of breath,
but careful history reveals they are not having any airway obstruction but experiencing breathlessness during the conversation because of the inefcient laryngeal closure and air leakage. They experience vocal fatigue due to the same mechanism.
The increased respiratory effort and laryngeal muscle activity to force glottal closure will result in fatigue. Exertional activities which require glottic closure like
lifting weight, pulling, and pushing may be difcult for some patients.
The quality of the voice in a poorly compensated vocal fold paralysis is harsh
and breathy due to the air escape. With time the quality improves due to the development of supraglottic compensatory strategies, especially in males. These patients
compensate with false cord adduction or apposing epiglottis to arytenoids in an
anterior-posterior dimension. These compensations will result in a rough, lowpitched voice. In females, there is a compensatory strategy of developing unnatural
high-pitched voice referred to as “paralytic falsetto” which is a result of contraction
of the ipsilateral cricothyroid muscle. Some patients exhibit symptoms of aspiration
such as cough on taking food especially liquid.
Fiberoptic laryngoscope examination will demonstrate various patterns of vocal
fold immobility (Figs.12.1 and 12.2). Indirect laryngoscopy with a mirror and rigid
scope; 70 or 90° can also help, but not as good as beroptic laryngoscope. Tongue
Fig. 12.1 Post
thyroidectomy left vocal
cord palsy
162
Fig. 12.2 Post
thyroidectomy left EBSLN
palsy
J. R. Menon and M. E. Issac
protrusion and grasping the tongue with gauze while performing rigid scopy affect the
natural state of vocal fold mobility. The affected vocal fold exhibits different positions. The affected vocal fold may lie in any position depending upon the degree of
re-innervation and synkinesis. It can either be an immobile vocal fold- paralysis, in
abducted or paramedian position or a vocal fold with restricted adduction or abduction-paresis. When the affected vocal fold is at an adducted position hoarseness may
improve over time because of the compensation of the unaffected vocal fold.
There are certain useful tasks applied during beroptic examination rather than
checking vocal fold mobility alone. One such task is the “eee-sniff” maneuver in
which the patient alternates between phonating the vowel “eee” and snifng and by
this a better judgment on the degree of impairment is possible. In patients with a
compensatory supraglottic contraction or dysphonia plica ventricularis which can
obscure the view of true vocal folds another phonatory task will help. This is called
“unloading” described by Koufman removes the supraglottic phenomenon. The
patient is instructed to hum through the nose or phonate with a sigh.
A strobe can be connected to the beroptic laryngoscope for a complete work- up. It
may show incomplete closure or a large glottal gap or increased amplitude of vibration.
Maximum phonation time (MPT) is another test to evaluate glottic insufciency.
Here the patient is instructed to take a deep breath and phonate the vowel “ee” for
as long as possible. MPT will be reduced in vocal fold palsy depending upon the
degree of glottis insufciency.
The prognosis depends upon the type of injury as well as the time elapsed
since onset.
In the immediate post-operative period, the supraglottic swallowing technique
(holding breath while swallowing) will avoid cough and make the swallowing better.
Voice therapy helps rehabilitate the weak voice in the postoperative period. And
it can help the patient to avoid developing wrong compensatory techniques and
subsequent muscle tension dysphonia. There are indirect and direct therapy procedures. Indirect therapy aims at improving vocal hygiene, counseling, and correcting
posture. Direct therapy aims at normalizing the expiratory force, enhancing vocal
12 Management ofVocal Fold Palsy inThyroid Surgery
163
projection, and optimizing medial compression of the affected vocal fold. Attempting
high-pitched phonation and turning the head towards the side of paralysis and in
opposite direction for paresis will enhance effective glottis closure and make the
voice better. All these are employed in the scenario when the surgeon is sure about
the integrity of the nerve. Methylcobalamin can be given. It has been claimed that it
improves regeneration of the injured nerve. Intravenous steroids can be given to
reduce the edema and speed up recovery.
While in an unfortunate event of a conrmed unilateral nerve injury such as
transection of the nerve during surgery, non-selective reinnervation can be done
which will retain the tone of the adductor muscles and help the vocal fold to attain
adduction dynamically. Ansa cervicalis to strap muscles is the nerve of choice. The
donor nerve is in the same eld and it is a powerful adductor motor nerve. A segment of the desired length is dissected and released from the surrounding fascia and
brought to the stump of recurrent laryngeal nerve above the point of injury near its
entry point. Nerve to nerve anastomosis is done using 7-o nylon or PDS.Fat or a
sheath of the vein is harvested to cover the area of microvascular anastomosis.
Tissue brin glue is optional and can be used to reinforce the anastomotic site.
In unilateral paralysis, the aim is to medialize the paralyzed vocal fold to improve
glottal closure. There are static procedures where we medialize the immobile vocal
fold and dynamic procedures where nonselective reinnervation or selective reinnervation to the adductors are done (Fig 12.3). It can be combined with a static procedure like medialization. Non-selective re-innervation with medialization procedures
like injection laryngoplasty or medialization thyroplasty is the procedure of choice
when the vocal fold failed to normalize in 6–8months.
In those who cannot wait for 6months and in those with aspiration-related morbidity injection laryngoplasty is the choice. The medialization procedures are
selected based on the position of paralyzed vocal fold from the midline as well as the
time of vocal fold palsy. When the time of palsy is within 6–8months an injection
Fig. 12.3 Nonselective
reinnervation ansa
cervicalis and
RLN.Thyroplasty implant
also seen
164
J. R. Menon and M. E. Issac
laryngoplasty, i.e. endoscopic paraglottic fat injection which is done under GA is the
choice. There are ofce procedures that can be done under direct vision of a exible
endoscope where hyalase or hydroxylapatite is injected into the paralyzed cord.
When the duration of paralysis is more than 6–8months then a laryngeal framework surgery is the preferred treatment. Type 1 thyroplasty (medialization thyroplasty) where a silastic implant is carved based on measurement of the window
made on the thyroid cartilage is inserted into the lower half of thyroid ala to medialize the affected vocal fold. The depth of medialization is assessed and the desired
depth is measured and the implant is carved. There are modications to this method
where a titanium screw is used in some centers. Laryngeal framework surgeries are
done under LA or MAC to assess the voice during surgery. Arytenoid rotation or
adduction is combined in some situations where the paralyzed vocal fold is at an
abducted position. A preoperative workup will decide whether the patient requires
arytenoid adduction and medialization thyroplasty. A maximum phonation time of
fewer than 6s, the presence of aspiration, extremely breathy voice, and a negative
medial compression test make the criteria for arytenoid adduction along with Type
1 or medialization thyroplasty (Figs.12.4 and 12.5).
Fig. 12.4 Medialization
thyroplasty right side—
silastic implant
Fig. 12.5 Arytenoid
rotation 4-0 prolene suture
through the muscular
process of left arytenoid
12 Management ofVocal Fold Palsy inThyroid Surgery
165
12.5 Bialteral Vocal Fold Palsy
Thyroidectomy continues to be the most common cause of bilateral vocal fold palsy
[7]. The severity of clinical features depends upon the nal position of the paralyzed
vocal fold. In some, it will be a breathy voice and a weak cough to start with but
eventually progress to snoring, noisy breathing, and saturation fall and end up in
reintubation.
Bilateral vocal fold palsy following thyroidectomy requires knowledge to understand the emergency of different ranges of insufcient glottic spaces, experience to
manage airway emergencies, and counseling the patient and bystander.
The initial part of the assessment requires exible endoscopic evaluation of the
status of the paralyzed vocal folds. This part is very important to correlate with the
symptoms and other signs to decide on emergency management.
When the symptoms are mild and the vocal folds show some amount of movement or one side is having only a paresis one can still handle the situation with a
propped-up position, O2 mask, and C-PAP, intravenous steroids, methylcobalamin.
Moderate to severe symptoms not getting relieved with steroids and C-PAP
should be planned for a temporary lateralization procedure like suture cordopexy of
the least mobile or immobile cord.
Tracheostomy continues to be the most common treatment to provide airway
without any compromise on voice and swallowing. The stigma associated with a
tracheostomy is living with a breathing tube in the neck is the only disadvantage.
Tracheostomy can be avoided in most cases since suture lateralization will provide
enough space for the airway without much compromise on the voice. In the endoscopic suture lateralization procedure, 3-0 or 4-0 proline suture is taken through the
thyroid cartilage, one above the vocal fold, another below the vocal fold, and endoscopically the sutures are then tied and pulled through the thyroid cartilage outer
lamina and xed over it. Here no tissue is removed. Suture lateralization provides
enough glottis space without much compromise on voice. The only disadvantage is,
it can cut through and reverse the effect of lateralization.
Arytnoidectomy is an irreversible method of lateralization where arytenoid cartilage is removed along with overlying mucosa. Coblator or laser can be used for
this purpose. This is the recommended treatment for pediatric cases.
A permanent procedure like endoscopic posterior cordotomy (Kashima’s procedure) assisted by laser or Coblator is required in an established case of BVCP who
have waited for more than 6–8months for the signs of recovery and in those to
establish a permanent airway and to decannulate those patients who have been tracheostomized for critical glottis space (Fig 12.6). Patients with longstanding glottis
stenosis can tolerate the insufcient glottic space. A permanent lateralization procedure like Kashima’s surgery can be combined with adenoidectomy in some situations. The technique involves making a transverse cut just anterior to the vocal
process with laser or Coblator. The tissue cut advanced along the same plane laterally till thyroid and cricoid inner perichondrium is reached. The ventricular band is
partially removed for better visualization and to expose thyroid cartilage. Routine
tracheostomy is not required in many cases. This can provide a better airway without much compromise on voice. The postoperative period is uneventful in most
166
Fig. 12.6 Post
thyroidectomy bilateral
vocal cord palsy after
Kashima’s posterior
cordotomy right side
J. R. Menon and M. E. Issac
cases. The cases without a tracheostomy can be monitored in the ICU for 24–48h.
Nebulization with adrenaline and intravenous antibiotics and steroids helps in
reducing the edema at the operated site. Temporary aspiration especially to liquids
has been noted in a few cases in the immediate postoperative period.
Most recently selective reinnervation for BVCP is getting appreciation since it
can provide dynamic movement and lost tone to the vocal folds. The only disadvantage is the waiting period and in some patients a temporary or permanent lateralization procedure is required in the waiting period.
The phrenic nerve is the donor nerve for abductor muscle and the nerve to thyrohyoid or ansa can provide the adductor function to the adductors.
12.6 External Branch ofSuperior Laryngeal Nerve (ExSLN)
Because of difculty in recognizing the subtle symptoms, injury to the superior
laryngeal nerve is less documented. ExSLN or Nerve of Gali Curci supplies the
cricothyroid muscle which tenses the vocal fold and helps in raising the vocal pitch.
The nerve is at risk during upper pole dissection because of its close relationship
with the superior thyroid vessels.
Anatomy: The superior laryngeal nerve (SLN) arises from the nodose ganglion
of the vagus nerve and in its downward course at the level of the internal carotid
artery it divides into internal and external branches. The internal branch runs inferior to the greater cornu of the hyoid, pierces the thyrohyoid membrane to innervate
laryngeal mucosa. The external branch travels along the inferior constrictor muscle
to reach the cricothyroid muscle. The nerve crosses superior thyroid vessels posteriorly near the superior pole of the thyroid gland.
Cernea etal. proposed their classication of ExSLN position in relation to the
superior pole of the thyroid gland or the superior thyroid vessels and it is as follows [8]:
Type 1: The nerve crosses the superior vessels more than 1cm above a plane tangent
to the edge of the superior pole.