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7 Blue Laser Therapy ofVocal Fold Leukoplakia
precancerous laryngeal leukoplakia. Laryngoscope.
2017;127(1):153–8.
22. Ahn A, Wang L, Slaughter JC, Nguyen AM, Ossoff
RH, Francis DO.Serial full-thickness excision of dysplastic vocal fold leukoplakia: diagnostic or therapeutic? Laryngoscope. 2016;126(4):923–7.
23. Zeitels SM, Akst LM, Burns JA, Hillman RE,
Broadhurst MS, Anderson RR. Ofce-based 532nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol.
2006;115(9):679–85.
24. Koufman JA, Rees CJ, Frazier WD, Kilpatrick LA,
Wright SC, Halum SL, etal. Ofce-based laryngeal
laser surgery: a review of 443 cases using three wavelengths. Otolaryngology. 2007;137(1):146–51.
25. Koss SL, Baxter P, Panossian H, Woo P, Pitman
MJ. Serial in-ofce laser treatment of vocal fold
leukoplakia: disease control and voice outcomes.
Laryngoscope. 2017;127(7):1644–51.
26. Hamdan AL, Ghanem A. Un-sedated ofce-based
application of blue laser in vocal fold lesions. J Voice.
2021;2021:S0892.
27. Miller BJ, Abdelhamid A, Karagama Y.Applications
of ofce-based 445nm blue laser transnasal exible
laser surgery: a case series and review of practice. Ear
Nose Throat J. 2021;100(1):105–12.
Blue Laser Therapy ofVocal Fold
https://t.me/medicina_free
Scars
8
8.1 Introduction
Aside from autoimmune and infectious diseases,
trauma is the most common cause of vocal fold
scars. Following injury, a three-phase response is
triggered leading to remodeling of the layered
structure of the vocal fold [1, 2]. Histologic
examination of vocal fold scars shows alteration
in the concentration and distribution of many
constituents of the lamina propria. In the acute
phase there is increase in procollagen synthesis,
whereas in the chronic phase there is increase in
collagen formation and decrease in elastin.
Collagen bers are described as thick bundles
and elastic bers as broken, dispersed with no
clear orientation [3]. Other extracellular matrix
constituents are also affected in the remodeling
process following injury. There is an increase in
bronectin, an adhesive molecule that helps regulate the architecture of the lamina propria, and a
decrease in decorin, a proteoglycan of crucial
importance in scar formation. There is also redistribution of hyaluronic acid across the different
layers of the lamina propria with decrease in its
total concentration. Vocal fold scars vary in
severity and anatomic conguration. According
to the American Laryngological Association and
European Laryngological Society, they are classied into 4 types: type 1 is limited to the lamina
propria without involvement of the mucosal lining, type 2 involves the mucosa, lamina propria,
and vocalis muscle, type 3 involves the anterior
commissure, and type 4 extends rostro-caudally
and antero-posteriorly [4].
The histologic changes in vocal fold scars are
invariably accompanied by alterations in the viscoelastic properties of the vocal fold and hence in
voice quality. The voice is characterized by a disturbance in pitch and/or loudness. Affected
patients usually report an increase in effort to talk
and voice fatigue which markedly impair their
communication skills. Other reported symptoms
include frequent throat clearing, globus sensation, and dysphagia. Laryngeal videostroboscopic examination shows a decrease or absence
of mucosal waves at the site of the scar with
phase asymmetry. Other ndings include bowing
of the vocal fold with incomplete glottic closure
during phonation. In severe cases, a defect or loss
of tissue may be observed at the free edge of the
vocal fold. On acoustic analysis, there is an
increase in the perturbation parameters (jitter and
shimmer), noise-to-harmonic ratio, and voice tur-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35283- 6_8. The videos can be
accessed individually by clicking the DOI link in the
accompanying gure caption or by scanning this link with
the SN More Media App.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
A.-L. Hamdan et al., Blue Laser Surgery in Laryngology,
https://doi.org/10.1007/978-3-031-35283-6_8
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8 Blue Laser Therapy ofVocal Fold Scars
bulence index. In addition, there is a decrease in
maximum phonation time and an increase in subglottic pressure, particularly in case of glottic
insufciency [5].
The treatment of vocal fold scars is daunting.
A multidisciplinary approach is often needed to
improve voice outcome. Voice therapy is effective in mild cases, and exercises such as chanting, maximum phonation time exercises, and
semi- occluded exercises are helpful in restoring
the malleability of the vocal fold cover. Therapy
that targets laryngeal hyperfunction is also useful [6]. In subjects who fail voice therapy, surgery is the mainstay treatment. This includes
scar excision, insertion of grafts such as fascia or
fat, laryngeal framework surgery/thyroplasty
type 1, injection laryngoplasty, and steroid injections [7–13]. Other options such as stem cell
therapy and broblast growth factors therapy
may be offered in selected cases [14–16]. Over
the last two decades, laser therapy has also
gained popularity as a treatment option. The
most used lasers are the photoangiolytic lasers,
namely the potassium titanyl potassium (KTP)
laser with a wavelength of 532 nm and the
pulsed-dye laser (PDL) with a wavelength of
585nm. The improvement following laser therapy has been ascribed to upregulation in extracellular matrix metalloproteinase (MMP)
mediators [17, 18]. Another suggested mechanism for the improvement is the formation of
cleavage plane between the basement membrane
and the underlying lamina propria [17]. Sheu
etal. investigated the utility of KTP laser in augmenting wound healing in a rat model and
showed a 200% increase in IL-1b gene expression. There was also an increase in MMP-1 and
MMP-2 gene expression at 1 week. MMPI-1 is
an enzyme responsible for the breakdown of collagen types I, II, and III, and MMP-2 an enzyme
responsible for the breakdown of collagen types
IV and V [19]. Zhang et al. examined KTPinduced inammatory response in vocal fold
scar of rabbits and showed that at 6W power,
KTP laser can cause a decrease in collagen type
1 A1 and collagen type 3 A1 formation. The
decrease in collagen type 1 formation is known
to improve the viscoelastic properties of the
vocal fold. In addition, there was downregulation of the inammatory response in comparison
to scar tissue treated with Nd-YAG and scar tissue not treated with laser. The authors concluded
that KTP laser treatment can lead to alteration in
the extracellular matrix constituents of the lamina propria [18].
The introduction of the endoscope with a
working channel and the advent of glass bers
have hastened ofce-based laser therapy of vocal
fold scars. In 2008 Mortensen etal. reported their
experience with PDL in 11 patients with vocal
fold scars who underwent 3 serial ofce-based
treatment. The authors noted marked improvement in the subjective and acoustic measures in
10 of the 11 patients [20]. Wang et al. reported
their experience in 18 patients with vocal fold
scars who were treated using the KTP laser in
near-to-contact mode (2–5 mm away from the
vocal fold) and showed a decrease in the VHI-30
score. There was also improvement in mucosal
waves and glottic closure 2 months following
treatment. The authors noted that patients with
type 1 and 2 vocal fold scars had more improvement than those with type 3 and 4 [21]. In a
multi-institutional review on the application of
KTP in ofce-based laryngeal surgery, Sheu
etal. advocated the use of KTP laser in various
pathologies of the vocal fold including scars. The
authors reported improvement in mucosal waves
and vocal fold closure during phonation in 90%
of the patients following treatment [22].
8.2 Case Presentations
8.2.1 Case 1: Left Fibrotic Vocal
FoldMass
A 21-year-old female professional singer with
migraine, asthma, anxiety, and stable LPR presented with dysphonia that had persisted after
voice therapy. She had bilateral vocal fold steroid
injection and left fascia implant for the left vocal
fold paresis. However, she still had dysphonia
due to left vocal fold post-hemorrhagic mass and
scar at the junction of anterior/middle of the left
vocal fold. In the operating room, good visualiza-
8.2 Case Presentations
https://t.me/medicina_free
tion with a medium female Sataloff laryngoscope
showed the dense brosis and fullness in the left
sticking area (Fig. 8.1). Prominent varicosities
along the superior surface of the left vocal fold
were cauterized blue laser in non-contact mode at
6 W, 40 ms pulse time, 300 ms pulse pause
(Fig.8.2). The left vocal fold mass was vaporized
using a blue laser submucosally starting in the
superior surface of the mass in contact mode
(Fig. 8.3, Video 8.1). A total 21 J were used.
Dexamethasone was injected to the resection
area. At the end of the procedure, the left vocal
fold was soft. Her one-week post-operation view
demonstrated soft vocal fold (Fig.8.4).
85
Fig. 8.3 Intraoperative microscopic view showing blue
laser using to resect the brotic mass submucosally
Fig. 8.1 Intraoperative view showing dense brosis fullness in the left vocal fold sticking zone. (Video 8.1
Surgical video showing blue laser using to vaporize left
vocal fold mass submucosally)
(▶ https://doi.org/10.1007/000- ant)
Fig. 8.4 Laryngeal examination showing soft vocal fold
1-week after the surgery
8.2.2 Case 2: Left Vocal Fold
A 36-year-old female teacher presented with dysphonia due to bilateral vocal fold scar. Laryngeal
microscopy with palpation demonstrated bilateral vocal fold ectasia and left brotic mass in the
mid-portion of left vocal fold (Fig. 8.5). Blue
laser was used at 6 W, 40 ms pulse time, 300 ms
pulse pause. The laser was used superiorly and
Fig. 8.2 Intraoperative microscopic view showing blue
laser using to vaporize the prominent varicosities. (Video
8.2 Video showing left anterior vocal fold scar disruption
using blue laser) (▶ https://doi.org/10.1007/000- ans)
laterally on the nodular mass to shrink it internally with minimal trauma of the vibratory margin (Fig. 8.6). Both vocal folds were injected
with a mixture of 5 uorouracil and triamcino-
FibroticMass
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Fig. 8.5 Intraoperative microscopic view showing left
brotic mass in the mid-portion of left vocal fold
8 Blue Laser Therapy ofVocal Fold Scars
Fig. 8.7 Intraoperative view showing vaporization of
vocal fold ectasia using blue laser
Fig. 8.6 Intraoperative view showing blue laser using
superiorly and laterally to shrink the mass
lone blue laser was also used to cauterize bilateral ectasias (Fig. 8.7). The patient was
re-evaluated 4 months after surgery. There was
signicant improvement with good vocal fold
vibratory motion and no mass recurrence
(Fig.8.8).
8.2.3 Case 3: Left Vocal Fold Scar
A 38-year-old female singer with history of left
vocal fold mass and hemorrhage presented with
dysphonia due to left mid vocal fold brotic
mass with scar despite having had voice therapy,
multiple laryngeal procedures including submu-
Fig. 8.8 Laryngeal examination showing no brotic
mass recurrence 6 months after laser treatment
cosal resection of the left vocal food mass, 5
uorouracil injection with triamcinolone KTP
vaporization of ectasia and cymetra injection. In
the operating room, there was still ectasia and
scar in the left mid and anterior vocal fold
(Fig. 8.9). The brotic scar was injected with
Amniox (growth factor). There was a little
8.2 Case Presentations
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Fig. 8.9 Intraoperative view showing ectasia and scar in
the left mid and anterior vocal fold
87
Fig. 8.12 Intraoperative view showing ectasia vaporizing using blue laser
Fig. 8.10 Intraoperative view showing disruption of left
vocal fold scar using blue laser
Fig. 8.11 Intraoperative view showing disruption of left
vocal fold scar using blue laser
Fig. 8.13 Intraoperative microscopic view showing soft
left vocal fold at the end of the surgery
brotic scar that did not respond to intralesional
injection. Blue laser was used at 6 W, 40 ms
pulse duration, 300 ms pulse pause in contact
and non-contact mode to disrupt this scar in 4
different locations (Figs. 8.10 and 8.11; Video
8.2). Blue laser was used to vaporize varicosities
and ectasia of the left vocal fold (Fig.8.12). A
total 7.3J were used. The left vocal fold was soft
at the end of the procedure (Fig. 8.13). The
patient reported improvement with her voice,
she received 2 more Amniox injections. Her
6-months post-op view (Fig.8.14).
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Fig. 8.14 Laryngeal examination showing improvement
of the left vocal fold stiffness and vibration 6 months after
the surgery
References
1. Ehrlich H. Collagen considerations in scarring and
regenerative repair. In: Garg H, Longaker M, editors.
Scarless wound healing. NewYork: Marcel Dekker;
2000. p.99–114.
2. Thibeault SL, Gray SD, Bless DM, etal. Histologic
and rheologic characterization of vocal fold scarring.
J Voice. 2002;16(1):96–104.
3. Rousseau B, Hirano S, Scheidt TD, et al.
Characterization of vocal fold scarring in a canine
model. Laryngoscope. 2003;113(4):620–7.
4. Hantzakos A, Dikkers FG, Giovanni A, et al. Vocal
fold scars: a common classication proposal by the
American Laryngological Association and European
Laryngological Society. Eur Arch Otorhinolaryngol.
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5. Moore JE, Sataloff RT.Vocal fold scar. In: Sataloff
RT, editor. Professional voice: the science and art of
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2017. p.1605–10.
6. Behlau M, Murry T. Voice therapy for benign vocal
fold lesions and scar in singers and actors. Singer’s
Voice. 2008;117:472.
7. DeFatta A, DeFatta J, Sataloff RT. Laryngeal lipotransfer: review of a 14-year experience. J Voice.
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8 Blue Laser Therapy ofVocal Fold Scars
8. Kishimoto Y, Hirano S, Kojima T, etal. Implantation
of an atelocollagen sheet for the treatment of vocal
fold scarring and sulcus vocalis. Ann Otol Rhinol
Laryngol. 2009;118(9):613–20.
9. Neuenschwander MC, Sataloff RT, Abaza MM,
et al. Management of vocal fold scar with autologous fat implantation: perceptual results. J Voice.
2001;15(2):295–304.
10. Van den Broek M, Heijnen J, Hendriksma M, et al.
Bilateral medialization thyroplasty in patients with
vocal fold atrophy with or without sulcus. Eur Arch
Otorhinolaryngol. 2020;277(7):2023–9.
11. Lahav Y, Malka-Yosef L, Shapira-Galitz Y, et al.
Vocal fold fat augmentation for atrophy, scarring, and
unilateral paralysis: long-term functional outcomes.
Otolaryngol Head Neck Surg. 2021;164(3):631–8.
12. Mortensen M, Woo P.Ofce steroid injections of the
larynx. Laryngoscope. 2006;116(10):1735–9.
13. Mortensen M.Laryngeal steroid injection for vocal
fold scar. Curr Opin Otolaryngol Head Neck Surg.
2010;18(6):487–91.
14. Hirano S, Sugiyama Y, Kaneko M, etal. Intracordal
injection of basic broblast growth factor in 100
cases of vocal fold atrophy and scar. Laryngoscope.
2021;131(9):2059–64.
15. Mattei A, Magalon J, Bertrand B, etal. Cell therapy
and vocal fold scarring. Eur Ann Otorhinolaryngol
Head Neck Dis. 2017;134(5):339–45.
16. Hertegård S, Cedervall J, Svensson B, et al.
Viscoelastic and histologic properties in scarred rabbit vocal folds after mesenchymal stem cell injection.
Laryngoscope. 2006;116(7):1248–54.
17. Prufer N, Woo P, Altman KW. Pulse dye and other
laser treatments for vocal scar. Curr Opin Otolaryngol
Head Neck Surg. 2010;18(6):492–7.
18. Zhang J, Zhen R, Wei C.Potassium titanyl phosphate
laser-induced inammatory response and extracellular matrix turnover in rabbit vocal fold scar. Eur Arch
Otorhinolaryngol. 2018;275(6):1525–32.
19. Sheu M, Sridharan S, Paul B, et al. The utility of
the potassium titanyl phosphate laser in modulating vocal fold scar in a rat model. Laryngoscope.
2013;123(9):2189–94.
20. Mortensen MM, Woo P, Ivey C, et al. The use
of the pulse dye laser in the treatment of vocal
fold scar: a preliminary study. Laryngoscope.
2008;118(10):1884–8.
21. Wang J, Mao W, Fang R, etal. Use of 532nm potassium titanyl phosphate laser on vocal fold scars under
topical anesthesia: a pilot study. Ann Otol Rhinol
Laryngol. 2022;131(7):715–23.
22. Sheu M, Sridharan S, Kuhn M, et al. Multiinstitutional experience with the in-ofce potassium
titanyl phosphate laser for laryngeal lesions. J Voice.
2012;26(6):806–10.
Blue Laser Therapy ofLaryngeal
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Stenosis
9
9.1 Introduction
Laryngeal stenosis is partial or circumferential
narrowing of the laryngeal airway from congenital or acquired causes. The goals of treatment are
securing airway and maintaining or restoring
good voice quality.
Laryngeal stenosis may affect posterior laryngeal, supraglottic, glottic, and/or supraglottic
areas. In this chapter, we explore the use of blue
laser in the management of this disorder. In this
chapter, we discussed current information regarding multiple laryngeal stenosis and use of blue
laser in selected cases.
The posterior glottis includes the posterior
(cartilaginous) third of vocal folds, the posterior
commissure or interarytenoid region, cricoarytenoid joints, the posterior portion of cricoid lamina, the arytenoid cartilages, and overlying
mucosa [1]. The etiologies of posterior glottic
stenosis (PGS) or posterior laryngeal stenosis
include endotracheal intubation (the most common), external trauma, laryngopharyngeal reux
(LPR), inhalation injury, caustic aspiration/ingestion, foreign body ingestion/aspiration, tuberculosis, diphtheria, and other causes including
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35283- 6_9. The videos can be
accessed individually by clicking the DOI link in the
accompanying gure caption or by scanning this link with
the SN More Media App.
previous surgery. Traumatic intubation, repeated
intubations, prolonged intubation, large endotracheal tube size, the presence of reux or local
infection, and motion of the endotracheal tube
are risks factor for developing post-intubation
PGS.
PGS was stratied by Bogdasarian and Olson
into four grades [1]. Type I involves an interarytenoid scar band between the vocal folds that is
anterior to and separate from the interarytenoid
mucosa. Type II stenosis involves scar of the
mucosa or musculature of the posterior interarytenoid area. Type III involves unilateral cricoarytenoid joint xation, and type IV involves
bilateral cricoarytenoid joint xation [2].
Evaluation should include detailed exible
laryngoscopy and ideally rigid laryngoscopy.
Traditionally, such examination has been performed under general anesthesia. However,
advances in in-ofce surgery have made that an
option for selected patients. Laryngeal palpation
may be performed in-ofce under local anesthesia. Stroboscopy is also useful. It is optimal to
detect scarring of the vocal folds, the relative vertical height and tension of the vocal folds, to
assess cricoarytenoid joints, and to detect many
other subtle abnormalities. Bilateral vocal fold
paralysis and cricoarytenoid arthritis should be
considered in the differential diagnosis. Laryngeal
nerve function is determined best by electromyography (EMG) before planning surgical repair.
Identifying severe paresis or paralysis can have a
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
A.-L. Hamdan et al., Blue Laser Surgery in Laryngology,
https://doi.org/10.1007/978-3-031-35283-6_9
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9 Blue Laser Therapy ofLaryngeal Stenosis
major impact on surgical planning. Normal laryngeal EMG of immobile vocal folds could indicate
arytenoid dislocation or ankylosis rather than
paralysis. CT of the larynx can be helpful to
assess cricoarytenoid joints and to examine other
levels of airway stenosis and to determine arytenoid position. Pulmonary function testing provides objective measurement of the airway
obstruction and also provides useful data of
objective voice analysis with air ow studies.
Such information may be valuable diagnostically
and for outcomes assessment [2].
Affected patients may be asymptomatic or
may present with life-threatening upper airway
obstruction necessitating a tracheotomy.
Asymptomatic patients usually should not have
surgical intervention. The goal of treatment is to
maintain adequate airway while preserving or
restoring voice. In patients with tracheotomy, the
goal is having the tracheotomy tube removed.
Microscopic examination of the glottic surfaces,
palpation of the cricoarytenoid complex and posterior glottic region, and examination of the subglottis and trachea complete the assessment [3].
Type I stenosis, endoscopic procedures may be
sufcient for treatment. However open laryngeal
procedures may be needed for advanced cases,
particularly for those whom endoscopic surgery
has failed repeatedly.
Webs are another form of laryngeal stenosis.
Webs connect the vocal folds. They may be congenital or acquired. Anterior glottic webs commonly result from laryngeal surgery or intubation,
but they also can be caused by other trauma
including inhalation injury and external trauma.
They form when there is mucosal injury to the
anterior one-third of both vocal folds, especially
near the anterior commissure. Laryngeal webs
are often asymptomatic and usually cause no
voice or breathing problems. Asymptomatic
webs usually should be left undisturbed.
Symptomatic webs may present with dysphonia,
or dyspnea with or without stridor. Tracheotomy
is rarely necessary unless there is respiratory distress which usually occurs with very extensive
webs [4].
Preoperatively, it is essential to determine
whether the web is the main cause of dysphonia
following laryngeal injury. In many cases, dysphonia is the result of vocal fold scar. A laryngologist should determine whether the web is
symptomatic, and its longitudinal and vertical
extent. Complete laryngeal web assessment
should include strobovideolaryngoscopy and
commonly high-resolution CT scan.
Small symptomatic webs can be treated endoscopically. However, external approaches can be
used, when necessary, particularly for recurrent
webs. Endoscopic resection of a laryngeal web
may be completed with laser or traditional instruments. It is possible to treat a web successfully
endoscopically without placement of a keel or
stent in selected cases. Such treatment can be
performed in an operating room or ofce setting.
Recurrence may be minimal by having the patient
do snifng exercises post-operatively and by disrupting adhesion caused by surgery using cold
instruments or laser. However, in many cases, it
is necessary to place a laryngeal keel or stent to
prevent reformation of the web [5, 6].
Another form of laryngeal stenosis is subglottic stenosis. The subglottic area begins approximately 5mm below the vocal fold at the junction
of squamous and respiratory epithelium and
extends to the inferior border of the cricoid cartilage. Subglottic stenosis (SGS) may affect both
the soft tissue and cartilage of the endolarynx and
is the most common form of laryngeal stenosis. It
can be partial or complete narrowing of the
endolarynx. SGS may be congenital or acquired
[7, 8]. Congenital subglottic stenosis is caused by
inadequate recanalization of the laryngeal lumen
after completion of normal epithelial fusion at
the end of the third month of gestation. It is the
third most common congenital disorder of the
larynx after laryngomalacia and recurrent laryngeal nerve paralysis [9]. In the absence of a history of endotracheal intubation, after trauma or
other recognized causes of stenosis, SGS is considered to be congenital [10]. Typically, it is diagnosed during infancy and presents with stridor,
dysphonia, and respiratory distress that often is
severe enough to require tracheotomy.
The etiologies of acquired subglottic stenosis
include mechanical trauma from intubation or
tracheotomy (the most common cause in children
9.2 Case Presentations
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91
and adults), laryngopharyngeal reux (LPR),
Rheumatologic or autoimmune disease such as
granulomatosis with polyangiitis. Less common
causes include scleroma, amyloidosis, osteochondroid hamartoma, relapsing polychondritis,
respiratory infections, idiopathic, chondroradionecrosis after radiation therapy, inhalation injury,
and neoplasm [11].
The most common grading for the diagnosis
of subglottic stenosis is the Meyer-Cotton grading scale.
1. Grade 1 stenosis is lumen obstruction less
than 50%.
2. Grade 2 stenosis is lumen obstruction between
51% and 70%.
3. Grade 3 stenosis is lumen obstruction between
71% and 99%.
4. Grade 4 stenosis is complete lumen obstruc-
tion [11].
History, physical examination, radiologic evaluation, and endoscopic examination of the airway
and esophagus are all essential to evaluate SGS.A
24-hour pH impedance monitor examination
should be considered to evaluate possible laryngopharyngeal reux [12]. Quantitative documentation of voice function is helpful for many reasons.
It may identify voice characteristics that were not
detected during multidisciplinary team assessment. It also provides baseline information that
allows quantitative assessment of outcomes [13].
Management of subglottic stenosis in children
differs from that in adults, and some operations
useful in children generally are not applicable to
adults. The goal of treatment is establishing stable adequate airway while preserving serviceable
voice. However, management is always challenging. In severe subglottic stenosis, tracheotomy
may be required to secure the airway. Traditional
treatment of subglottic stenosis often has involved
tracheal resection and reanastomosis. However,
substantial mortality and morbidity are associated with this approach. Despite being effective
only temporarily in some patients, endoscopic
management may be appropriate and is used
commonly [14]. Laryngeal dilatation may be useful in the early stages of soft tissue stenosis for-
mation. The rst line of treatment is usually
endoscopic resection of stenotic lesions [15].
CO2 laser has been used with reasonable success in the management of early or mild subglottic stenosis cases and in selected cases with more
severe stenosis [16]. We have abandoned it almost
completely in favor of blue laser except in cases
of severe stenosis.
Application of Mitomycin-C, an antineoplastic antibiotic that acts as an alkylating agent by
inhibiting DNA and protein synthesis, may be
helpful in preventing recurrence, but results have
been mixed. Corticosteroids may be used locally
or systemically, but their value remains uncertain
[17]. The author (RTS) has had success with
injection of 5-uorouracil mixed with triamcinolone, but analysis of the results has not been completed. He also has found systemic methotrexate
to be helpful in some cases.
If endoscopic procedures are contraindicated
or unsuccessful, an open surgical procedure may
be performed. Options include but are not limited
to anterior cricoid split, posterior cricoid split,
external expansion surgery, and cricoid resection
with thyrotracheal anastomosis. Laryngotracheal
mucosal grafting also may be of value for some
patients and may be performed through an endoscopic or external approach [18].
9.2 Case Presentations
9.2.1 Case 1: Anterior Commissure
Sub-Cordial Web
A 27-year-old male with history of laryngeal
trauma with laryngeal fracture and anterior glottic
web and right vocal process avulsion and scar that
caused incomplete glottic closure. He had undergone multiple laryngeal procedures to improve
his breathing and voice. However, his laryngeal
examination still demonstrated bilateral abductor
paralysis, anterior commissure sub- cordial web,
immobilized left arytenoid, right vocal process
avulsion, and incomplete glottic closure. In the
operating room, a Sataloff female medium laryngoscope was used to achieve good visualization.
The anterior laryngeal web involved the vocal
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