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Vocal cord paralysis
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Current management trends
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7/18/2010
Dr. T. Balasubramanian
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1
By
The vagus nerve arises from three nuclei located in the medulla of brain. They are:
1. Nucleus ambiguous
2. Nucleus dorsalis
Nucleus ambiguus: Is the motor nucleus of the vagus nerve. It lies within the
medulla and is approximately 2 cm long in reticular formation of medulla. Superior
portion of the nucleus projects fibers to the 9th cranial nerve, while the middle
portion to the 10th nerve, and the inferior portion to the cranial part of the
11th cranial nerve. The efferent fibers of the dorsal nucleus innervates the
involuntary muscles of bronchi, esophagus, heart, stomach, small intestine, and
part of the large intestine. The efferent fibers of the nucleus of the tract of solitarius
carry sensory fibers from the pharynx, larynx, and esophagus.
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The vagus nerve (wanderer) takes a tortuous path after emerging from the jugular
foramen. It has two ganglions. The smaller superior ganglion and a larger inferior
or nodose ganglion. In the neck the vagus nerve runs behind the jugular vein and
carotid artery. It supplies the muscles of the pharynx and most of the muscles of
soft palate. It gives rise to the superior laryngeal branch. The right vagus nerve is
32 cm long, while the left nerve is 43 cm long. Due to these variations in the length
of vagus nerve, there could be a discernible lag in the movement of left vocal cord in
comparison with the right cord. To minimize this lag the left recurrent laryngeal
nerve is supposed to contain more larger and fast conducting nerve fibers.
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The axons of the recurrent laryngeal nerve are situated anteriorly in the vagus as it
exits from the brain stem. In the cervical segment of the vagus nerve the recurrent
laryngeal nerve axons congregate on its ventro medial aspect.
On the right side of the neck the vagus nerve passes over the subclavian artery. In
this region the right recurrent laryngeal nerve branches from the main trunk of
vagus and loops around the subclavian artery from anterior to posterior and travels
upwards in the neck towards the larynx. In rare instances (less than 1% of cases)
the inferior laryngeal nerve branches out of the vagus nerve directly and enters the
larynx at the level of the cricoid cartilage. This non recurrent inferior laryngeal
nerve crosses posterior to the common carotid artery and enters the larynx
posterior to the cricothyroid joint. This non recurrent laryngeal nerve is prone to
injuries if the surgeon is not aware of its possibility. This aberrant course of the
recurrent laryngeal nerve can be explained embryologically. Normally the
recurrent laryngeal nerves are pulled upwards in the neck around the 6th arches of
aorta on both sides. On the left side the 6th arch remains as ductus arteriosis and
later becomes the ligamentum arteriosum. On the right side the 6th aortic arch
normally resorbs during the embroyonic development causing the recurrent
laryngeal nerve to pass under the subclavian arch. In very rare instances this 4th
arch also get resorbed during embryonic development. This causes the right
subclavian artery to arise directly from the descending aorta and the right inferior
laryngeal nerve branches from the vagus and directly enters the larynx without
looping around any vascular structure.
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The recurrent laryngeal nerve as it ascends the neck courses from lateral to medial
till it reaches the tracheo oesphageal groove and then it enters the larynx. In a
quarter of patients this nerve may lie antero lateral to the tracheo oesophageal
groove where it could be endangered during thyroid surgeries. The left recurrent
laryngeal nerve arises from the main vagal trunk at the level of aortic arch where it
lies anterior to the bifurcation of left common carotid and subclavian arteries. It
then loops beneath the aorta lateral to the ligamentum arteriosum (which is a 6th
arch derivative) and ascends upwards and medially towards the larynx. In majority
of patients the recurrent laryngeal nerve courses via the mediastinum as a single
trunk one on either side till it reaches the cricoid cartilage. On rare occasions there
may be more than one main trunk on either side of the neck.
The following are the contributions made by the recurrent laryngeal nerve:
According to Katz about 40% of recurrent laryngeal nerves divided before entering
the larynx. During surgery in order to avoid damaging this vital nerve a surgeon
should always safely assume that there are more than one branch of this nerve close
to the larynx.
Historically much importance has been given to the relationship of the recurrent
laryngeal nerve with that of inferior thyroid artery. Some authors go to the extent
of identifying this nerve by identifying the inferior thyroid artery. It should be
stressed that this relationship is purely conjectural and does not lend itself to broad
generalizations. The left recurrent laryngeal nerve has been described to course
deep to the inferior thyroid artery in majority of cases while the right has been
shown to pass deep to, superficial to or between the branches of recurrent laryngeal
nerves in equal proportions.
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laryngeal nerve. This close relationship with that of inferior thyroid artery places
the nerve at great risk during surgery if there is bleeding from this area.
This nerve has also been shown to have varying relationship to that of Berry's
ligament. It may course lateral, medial or through this ligament.
The only reliable landmark of recurrent laryngeal nerve close to thyroid is the
cricothyroid articulation. The recurrent laryngeal nerve passes posterior to this
joint to enter the larynx.
1. Galen's anastomosis
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4. Cricoid anastomosis
5. Thyroarytenoid anatomosis
6. Thyroid foramen
7. Cricothyroid anastomosis
Figure showing the various anastomotic points between the superior and recurrent
laryngeal nerves.
Superior laryngeal nerve: This nerve gives rise to two branches 1. Internal and 2.
external laryngeal branches. The internal laryngeal branch of superior laryngeal
nerve pierces the thyrohyoid membrane and supplies sensation to the larynx above
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the level of glottis. The external laryngeal branch of superior laryngeal nerve
innervates the cricothyroid muscle, which is the only laryngeal muscle not to be
innervated by the recurrent laryngeal nerve.
The right vagus nerve passes anterior to the subclavian artery and gives off the right
recurrent laryngeal nerve. This nerve loops around the subclavian artery to reach
the tracheo oesophageal groove. It accompanies the inferior thyroid artery for some
distance before entering the larynx behind the cricothryoid joint.
The left vagus does not give off the recurrent laryngeal branch until it reaches the
thorax. The left recurrent laryngeal nerve winds around the aorta posterior to the
ligamentum arteriosum. It ascends back towards the larynx in the tracheo
oesophageal groove.
Laryngeal musculature:
The muscles of larynx may be divided into extrinsic (muscles that attach the larynx
to neighboring structures) and intrinsic groups.
The intrinsic muscles of the larynx govern the movements of the vocal cords. These
muscles are innervated by the recurrent laryngeal nerve. The intrinsic muscles of
larynx have both their origin and insertion on the cricoid, thyroid or arytenoid
cartilages. These muscles act together to fulfill their functions i.e. respiration,
protection of larynx and vocalization. Studies have shown that each laryngeal
muscle is not a single entity but an assembly of anatomically distinct compartments
potentially adapted to serve different functions. These individual compartments
receive nerve supply from separate branches of recurrent laryngeal nerve.
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4. Oblique arytenoid: This muscle along with transverse arytenoid closes the
laryngeal inlet during the act of swallowing.
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1. Aryepiglottic folds
2. Vestibular folds
3. Vocal folds
The muscles controlling these sphincters are derived from the intrinsic muscles of
larynx. These sphincters can contract together or independently. All these
sphincteric components act in unison during the act of swallowing thus preventing
effectively any aspiration of food into the airway.
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The vestibular and vocal folds may oppose without closure of the aryepiglottic
sphincter. This can be observed during direct laryngoscopic examination.
The vestibular folds cannot be closed independently of the vocal folds, on the
contrary the vocal folds adduct without closure of the other two sphincters during
phonation.
Various theories have been proposed to explain the various positions assumed by a
paralyzed vocal cord.
Semon's law: This theory proposed by Rosenbach and Semon in 1881, depends on
the concept that abductor fibres in the recurrent laryngeal nerves are more
susceptible to pressure than the adductor fibers. After a number of amendments
this law is stated as " In the course of a gradually progressing organic lesion
involving the recurrent laryngeal nerve three stages can be observed. In the first
stage only the abductor fibers are damaged, the vocal folds approximate in the
midline and adduction is still possible. In the second stage the additional
contracture of adductors occur so that the vocal folds are immobilized in the median
position. In the third stage the adductors become paralysed and the vocal folds
assume a cadaveric position".
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involving the recurrent laryngeal nerve the abductors paralyze first followed by the
adductors. When recovery takes place the first muscle group to recover will be the
adductors before the abductors could recover.
Differential innervation theory: This theory was based on the anatomic fact that the
recurrent laryngeal nerve often branched outside the larynx. Injury to individual
branches could cause paralysis of specific groups of muscles accounting for the
varying positions assumed by the paralysed cord.
Changes in the cricoarytenoid joint and paralysed muscles: These changes have
been proposed to explain the position of the cord in vocal fold paralysis. This theory
of progressive fibrosis of muscles has no anatomical proof.
Wagner and Grossman theory: This is the most popular and widely accepted
theory which could account for the varying positions assumed by a paralysed vocal
cord. This theory was first proposed by Wagner and Grossman (1897). This theory
states that in complete paralysis of recurrent laryngeal nerve the cord lies in the
paramedian position because the intact cricothyroid muscle adducts the cord.
(Because the superior laryngeal nerve is intact). If the superior laryngeal nerve is
also paralysed the cord will assume an intermediate position because of the loss of
adductive force. This theory has been confirmed by electro myological studies.
According to this theory, chest lesions should cause recurrent laryngeal nerve
paralysis alone, but in many patients with lung cancer the cord assumes a
intermediate position. This has been attributed to the phenomenon of retrograde
atrophy of the vagus nerve up to the level of nucleus ambiguus.
Paralysed vocal cords may demonstrate some movement due to the action of
interarytenoid muscle which gets bilaterally innervated.
Recent studies pertaining to laryngeal innervation has shown that the superior and
recurrent laryngeal nerves have more interconnections then the oft repeated Galen's
anastomosis. Anatomical studies have demonstrated that superior laryngeal nerve
contributes motor fibers to intrinsic laryngeal muscles other than cricothyroid.
Some of the intrinsic muscles of larynx have more than one belly with differing
nerve supplies.
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Vocal cord paralysis is a sign of disease and is not a diagnosis. It may be due to a
lesion anywhere from the cerebral cortex to the neuromuscular junction. Because
of the large size of the nucleus ambiguus, small lesions in it may produce isolated
laryngeal and pharyngeal motor losses. Lesions involving the nucleus ambiguus
may cause bilateral paralysis more often than unilateral palsy.
Peripheral damage to the laryngeal innervation may be of three types:
1. Damage to the vagus trunk above the nodose ganglion, the origin of superior
laryngeal nerve
2. Damage to the vagus nerve below the level or to the recurrent laryngeal nerve
Congenital vocal cord palsy: Many infants with stridor may have congenital
paralysis of vocal cords. This could occur with or without other associated
abnormalities (i.e. neurologic, laryngeal and cardiac defects). The most commonly
associated anomaly in these patients is the presence of hydrocephalus. The
mechanism of vocal cord palsy in these children is still not clear. It could be due to
stretching of the vagus nerve, due to complicated delivery etc.
Table showing the probable acquired causes of vocal cord palsy along with their
incidences:
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Malignant disease: One third of all vocal cord paralysis is caused by malignancies
like lung cancer, oesophageal cancer and thyroid malignancies. Other rare causes
could include temporal lobe malignancies, posterior fossa tumors, paragangliomas
etc.
Surgical trauma: is the second commonest cause of vocal cord paralysis. Thyroid
surgeries are the commonest. Mediastinal surgeries, oesophageal surgeries can also
cause vocal cord palsy.
The following are the surgeries known to cause recurrent laryngeal nerve paralysis:
3. Other surgeries / procedures: Skull base surgery, brain stem surgery, central
venous catheterization and endotracheal intubation.
Neurologic causes: Include brain stem ischemia, multiple sclerosis and head
injuries.
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Superior laryngeal nerve: This branch from the vagus supplies the main sensory
innervation of larynx in the glottic and supraglottic regions with some minimum
contribution to posterior subglottic area. It branches out of the vagus nerve just
below the nodose ganglion. It is branched from the medial aspect of the vagus
nerve. It lies superficial to the superior cervical ganglion form which it receives
sympathetic supply. This nerve also supplies the carotid body. Its motor
innervation supplies the cricothyroid muscle. Traditional belief is that paralysis of
superior laryngeal nerve causes bowing and flaccidity of true vocal cords with
decreased vocal range and laryngeal rotation. According to Sulica this premise is
not entirely accurate. In human larynx the superior laryngeal nerve has complex
functional inter relationship with the recurrent laryngeal nerve. Hence the degree
of compensation of these two nerves following injury is not entirely straight
forward.
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The average length of superior laryngeal nerve is about 2 cm in males and 1.5 cms
in females. It divides into an internal and external laryngeal branches.
Kierner classified the superior laryngeal nerve into 4 types depending on the
relationship of its external branch to the superior pole of thyroid gland.
Type I nerve: In this type the external branch of superior laryngeal nerve cross the
superior thyroid artery about 1cm above the superior pole of thyroid gland.
Type II nerve: In this type the external branch of superior laryngeal nerve crosses
the superior thyroid artery within 1 cm of the superior pole of thyroid gland.
Type III nerve: In this type the external branch of superior laryngeal nerve crosses
the superior thyroid artery under cover of the superior pole of thyroid gland.
Type IV nerve: In this type the external branch of superior laryngeal nerve
descends dorsal to the superior thyroid artery and crosses its branches just superior
to the upper pole of thyroid gland.
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Awareness of these anatomical variations will help the surgeon in preserving this
branch during head and neck surgeries.
The external branch of the superior laryngeal nerve divides into two branches and
supplies the oblique and rectus bellies of cricothyroid muscle. It should be borne in
mind that this nerve pierces the inferior constrictor of pharynx before supplying the
cricothyroid muscle.
Clinical features:
These patients have very slight voice change. Patients may even complain of
hoarseness of voice. Singers find it difficult to maintain the pitch. Diplophonia is
common in these patients (defect in the production of double vocal sounds). The
pitch range is decreased in these patients. This is due to the fact that cricothryoid
muscle is very important in maintenance of vocal cord tension and this muscle is
supplied by the superior laryngeal nerve.
On indirect laryngoscopy examination the vocal folds appear normal during quiet
respiration. There could be seen a deviation of the posterior commissure to the
paralysed side. The posterior commissure points towards the side of the paralysis.
At rest the paralysed vocal fold is slightly shortened and bowed and may lie at a
lower level than the opposite cord.
There is also associated loss of sensation in the supraglottic area causing subtle
symptoms like frequent throat clearing, paroxysmal coughing, voice fatigue and
foreign body sensation in the throat.
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1. Arytenoid oedema
Bilateral superior laryngeal nerve injury: Fortunately this condition is very rare. It
could result in fatal aspiration and pneumonia. This condition is infact difficult to
diagnose as there is no asymmetry between the vocal folds.
Unilateral superior and recurrent laryngeal nerve injury: This occurs usually in
high vagal or brain stem lesions. Vocal folds are in intermediate position and the
patient tends to have a breathy voice. There is also a tendency to aspirate.
Bilateral recurrent laryngeal nerve palsy: In this condition both cords assume a
paramedian position compromising the airway. This commonly occurs following
total thyroidectomy or in thyroid malignancies. The patient will commonly manifest
with stridor. The voice will be near normal.
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Bilateral superior and recurrent laryngeal nerve injury: Bilateral vocal cords are
intermediate, flaccid, and motionless. The patient experiences aphonia and is at
high risk for aspiration.
Examination of neck is a must in all these patients. Neck should be examined for
the presence of thyroid mass, cervical adenitis.
Evaluation:
The standard diagnostic workup and evaluation of a patient with vocal cord
paralysis of unknown etiology is as follows: CXR, cervical spine series, barium
swallow, thyroid scan, CT or MRI of head, neck, and possibly thorax, CBC, Thyroid
function tests, ESR, Rheumatoid factor, Parathyroid hormone, calcium and glucose
levels, PPD, VDRL, fungal titers, lyme titers, and possibly a lumbar puncture.
Another adjuvant diagnostic aid to be considered is laryngeal electromyography.
Described by Miller et al in 1982, this method of evaluation of laryngeal muscle
innervation is gradually gaining acceptance by otolaryngologists. It is an analysis of
the electrical activity generated by a motor unit. It is performed percutaneously,
under local anesthesia on the cricothyroid muscles and thyroarytenoid muscles to
test both the superior laryngeal nerve and recurrent laryngeal nerve, respectively.
Miller, et al claims that laryngeal EMG is the most accurate method of determining
superior laryngeal nerve paralysis. It also appears to be helpful in cases of
mechanical fixation of the cords and predicting outcome of certain cases of
paralysis.
Videostroboscopy: Plays an important role in examining the vocal folds for mobility
disorders. This brings out the loss of mucosal wave pattern which is the earliest sign
of vocal fold disorder. It also shows incomplete closure with large glottic chinks in
patients with unilateral vocal fold paralysis. Paralyzed vocal folds show increased
amplitude of vibrations due to atrophied vocalis muscle. In cases of mild paralysis
of vocal folds the increased amplitude as seen in Videostroboscopy could be the only
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positive sign. This examination also helps in assessment of vocal fold height
differences and status of vocal process during phonation.
Maximal phonation time: Is a simple bedside test to assess the vocal cord status of a
patient. The patient is asked to take a deep breath and asked to phonate vowel “ee”
for as long as possible. Normal healthy adult can do it for 25 seconds. In patients
with vocal fold paralysis they may not be able to maintain it for more than 10
seconds because of phonatory waste.
Imaging has a very important role to play in the evaluation of causes for vocal cord
palsy. CT scan and MRI imaging of neck and thorax to rule out lesions that could
involve the recurrent laryngeal nerves in these areas must be performed.
3. Repetitive stimulation
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Diagnostic needle testing looks for the type of electrical activity both at rest
and during voluntary recruitment.
Fine wire electromyography uses multiple fixed fine wire electrodes. This
technique is used to examine patients with suspected synkinesis or laryngeal
dystonia.
Nerve injury leaves the muscle without innervation. The muscle fibers become
hypersensitive to acetylcholine causing them to discharge spontaneously. This is
evident when the muscle fibers are stimulated as in the case of insertion of needle
when laryngeal electromyography is being performed. Two primary wave forms
are generated. The first one is the positive sharp waves and the next one being
waves caused due to muscle fibrillation. The presence of these two waves indicates
that the muscle has lost its innervation, and is yet to be contacted by the
regenerating nerve sprout. It also indicates the muscle has not undergone fibrosis
due to lack of innervation. A fibrosed muscle due to lack of innervation is
prognostically bad.
When the muscle fibers are contacted by the sprouting nerve the nerve starts to
contract voluntarily under the influence of the regenerating nerve. Since these
newer sprouts have slow conduction rates the muscle fibers will be slightly delayed
in their action
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Large amplitude potentials recorded after vocal fold paralysis indicates that the
injury is old and stable.
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4. Normal recruitment
Management:
Decisions regarding the management of vocal cord paralysis are made on the basis
of the laryngeal function that is compromised due to the paralysis. In patients with
unilateral paralysis of vocal cords the voice is breathy and the patient faces risk of
aspiration due to compromised adduction of the vocal folds. In bilateral paralysis of
vocal folds the gravest cause for concern is total loss of abduction of both vocal folds
compromising the airway causing stridor. These patients usually have near normal
and functional voice. Some patients with unilateral recurrent laryngeal nerve
paralysis complain of shortness of breath while speaking. This should not be
confused with airway compromise. This is due to the fact that excess air leaks out of
the lungs while the patient speaks due to improper laryngeal seal. In order to
overcome this air leak some patients increase their respiratory effort and laryngeal
muscular activity causing increased strain to the vocal folds.
The voice of the patient should be recorded, since the major complaint is going to be
hoarseness of voice.
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Ideally speaking a wait and watch approach is useful in patients with unilateral
idiopathic paralysis of vocal cords. Spontaneous recovery is the order of the day in
these patients. The wait period may last up to 6 months in some patients.
1. Speech therapy
3. Intracordal injections
4. Selective reinnervation
Speech therapy: Can be used alone or in conjunction with other surgical modalities
of management. Behavioral voice therapy is very helpful in rehabilitating a weak
and breathy voice. Voice therapy may be used as a standalone treatment of with
other medical modalities of treatment.
Before beginning speech therapy the pitch, loudness and quality of voice should
be evaluated. Breathiness, reduced loudness and a weak cough have been associated
with leakage of air through glottis.
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The various compensatory mechanisms which are evident in patients with vocal
cord palsy should be considered. Patients may use these maneuvers to help voice
but they place strain on the voice mechanism inadvertently.
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Posture changes, reduction of muscle tone will go a long way in improving the
therapeutic result.
Direct procedures
Indirect procedures
The best way to decrease expiratory drive is to encourage the patient to speak in a
quiet and confident tone. When a patient is speaking in a quiet and confident voice
the air pressure and air flow match the resistance of vocal folds.
Surgical medialisation:
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and further developments were not introduced until the 1950's. Several authors
then introduced different modifications but the procedure did not become popular
until the late 1970's when Isshiki introduced his thyroplasty technique. This
involved displacing and stabilizing a rectangular, cartilaginous window at the level
of the vocal cord, therefore pushing the soft tissue medially. This technique gained
wider acceptance after Isshiki reported the successful use of Silastic as the implant
material. Silastic works very well because it is easier to carve than cartilage and can
be tailor made for each patient.
The technique is performed under local anesthesia to allow the patient to phonate
during the procedure. Thus, the degree of medialization can be determined
immediately, intraoperatively by the quality of the patient's voice. A horizontal skin
incision is made overlying the mid-thyroid ala. A window is made in the thyroid
cartilage on the involved side corresponding with the level of the true vocal cord.
The Silastic implant is then carved (many different modifications) to approximate
the defect. A subperichondrial window is made in the endolarynx, and the Silastic
implant is inserted into the window. The implant is fashioned so that is it wedged in
place, therefore no suturing is required. The quality of the patient's voice is checked
and glottic closure can be assessed using flexible endoscopy. If the desired voice is
not obtained, or the airway is impaired, the implant can easily be removed and
another redesigned.
Complications:
1. Airway compromise
2. Wound infection
3. Hematoma
4. Extrusion of the implant
5. Laryngocutaneous fistula formation
1. Reversible
2. Can be effective even with fixed cord
3. The patient has immediate benefit
Disadvantages:
1. Skin incision
3. Results variable
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Intracordal injections:
Injection augmentation of vocal folds date back to 1911 when Brunings injected
paraffin via indirect laryngoscopy to medialize the immobile vocal fold.
Complications:
1. Airway edema
2. Granuloma formation
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Advantages:
Vocal fold injection for global augmentation of vocal fold is a successful way to treat
glottic closure insufficiency. Autologous fat is an excellent material for this purpose.
Advantages of fat:
Autologous fat injection is indicated only to close small / medium sized glottal gap.
This procedure is not useful in patients with more than 4 mm glottal gap or with
shortened / slackened vocal folds. Similarly this procedure is contraindicated in
patients with contralateral poor abduction of vocal cord.
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These patients should have adequate subcutaneous fat tissue for harvesting.
Fat harvesting:
Lipoinjection is usually performed using 18 or 19 gauge needle. Since the fat that is
to be injected is highly viscous pressurized injection devise like Brunning’s syringe
is preferred.
1. Lipid granuloma
This was first used in 1980’s. These injections just increase the bulk of the vocal
fold and in no way improves the mobility of the vocal fold. The main role of these
injections is to reduce the phonatory waste.
Originally Bovine collagen is used for these injections. Main advantage of collagen
over fat injection is the ease with which collagen can be injected. Major problem
with bovine collagen is the risk of graft rejection because it is a xenograft.
Now autologous collagen can be harvested from the skin of individuals and used to
inject the paralyzed cord.
Use of micronized acellular dermis to be injected into the paralyzed vocal fold:
This material is available since the year 2000. It is a product of human organ
donation. The dermis is harvested from the torso and legs of cadavers following the
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protocol of organ donation. The material harvested should be checked for HIV and
Hepatitis infections.
Other materials that can be injected to increase the bulk of the paralysed cord
include:
1. Calcium hydroxyapatite
2. Hyaluronan
Selective reinnervation:
Nerve-Muscle Transfer:
Originally described by Tucker in 1977, this procedure uses a branch of the ansa
hypoglossi attached to a small block of omohyoid muscle as a nerve-muscle pedicle
to innervate the thyroarytenoid muscle on the involved side. The procedure is based
on the strap muscles being accessory muscles of respiration. Prerequisite to
reinnervation is a mobile cricothyroid joint, and that the cause of the paralysis has
not left the ansa hypoglossi denervated as well.
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The results of this procedure have been very good. Tucker reports an 80%
success rate, and other authors (May and Beery) have reported similar results.
Granted, there is a delay, usually 2-6 months before voice improvement begins.
Advantages:
Disadvantages:
1. Skin incision
Medialization thyroplasty:
Payr in 1915 first described this procedure. He created an anterior based cartilage
flap overlying vocal folds and pushed it medially. Medialization thyroplasty is
performed commonly these days for unilateral vocal fold paralysis with a large
glottic chink.
Indications:
Gortex / silastic block can be used to hold the medialized cartilage flap.
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The initial aim is to secure the airway as these patients will manifest with stridor. A
tracheostomy should be performed on an immediate basis.
This involves several techniques that surgically widen the glottic opening. While
this improves the airway, the patient's
voice quality suffers. The three most commonly utilized techniques are
arytenoidectomy, arytenoidopexy, and cordectomy.
Arytenoidectomy:
Arytenoidopexy:
Involves displacing the vocal fold and arytenoid without surgical removal of any
tissue. It can be done endoscopically with a suture passed around the vocal process
of the arytenoid and secured laterally. This procedure, however, has a relatively
high failure rate.
Cordectomy:
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Reinnervation:
Anastomosis between the phrenic nerve and the damaged recurrent laryngeal nerve
has been attempted in patients with bilateral recurrent laryngeal nerve paralysis
with varying results.
This method is apparently more physiologic and dynamic in nature. This method is
rather useful in treating patients with bilateral abductor paralysis. Paced
stimulation of posterior cricoarytenoid muscle is performed using an implantable
stimulator. Care should be taken to ensure that the frequency of stimulation /
pacing should sync with the process of respiration.
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