subglottic stenosis in children
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Subglottic Stenosis in Children
Author: John E McClay, MD; Chief Editor: Arlen D Meyers, MD, MBA more...
Updated: Dec 6, 2011
Background
Subglottic stenosis (SGS) is a narrowing of the subglottic airway, which is housed in the cricoid cartilage. The image
below shows an intraoperative endoscopic view of a normal subglottis.
Intraoperative endoscopic view of a normal subglottis
The subglottic airway is the narrowest area of the airway, since it is a complete, nonexpandable, and nonpliable ring,
unlike the trachea, which has a posterior membranous section, and the larynx, which has a posterior muscular
section. The term subglottic stenosis (SGS) implies a narrowing that is created or acquired, although the term is
applied to both congenital lesions of the cricoid ring and acquired subglottic stenosis (SGS). See the images below.
Grade III subglottic stenosis in an 18-year-old patient following a motor vehicle accident. The true vocal cords are seen in the
foreground. Subglottic stenosis is seen in the center of the picture.
Endoscopic view of the true vocal cords in the foreground and the elliptical congenital subglottic stenosis (SGS) in the center of
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the picture.
Subglottic view of very mild congenital subglottic stenosis. Laterally, the area looks only slightly narrow. When endotracheal tubes
were used to determine its size, it was found to be 30% narrowed.
Subglottic view of congenital elliptical subglottic stenosis.
Granular subglottic stenosis in a 3-month-old infant that was born premature, weighing 800 g. The area is still granular following
cricoid split. This patient required tracheotomy and eventual reconstruction at age 3 years. True vocal cords are shown in theforeground (slightly blurry).
Intraoperative laryngeal view of the true vocal cords of a 9-year-old boy. Under the vocal cords, a subglottic stenosis can be seen.
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This spiraling subglottic stenosis is not complete circumferentially. Laser therapy was the treatment choice and was successfulafter 2 laser treatments.
Continued lasering of the subglottic stenosis. The reflected red light is the aiming beam for the CO2 laser.
Postoperative view. Some mild residual posterior subglottic stenosis remains, but the child is asymptomatic and the airway isopen overall.
Preoperative view of a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Vocal cords are in theforeground.
A close-up view.
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Postoperative view. The patient had been intubated for 1 week and extubated for 1 week.
A subglottic view following dilation with an endotracheal tube to lyse the thin web of scar and a short course (5-day) treatment with
oral steroids.
Postoperative view of a 4-month-old infant with subglottic stenosis following cricoid split. Notice very mild recurrence of scaring atthe site of previous scar. Overall, the airway is open and patent. The anterior superior area can be seen, with a small area of
fibrosis where the cricoid split previously healed.
Preoperative subglottic view of a 2-year-old patient with congenital and acquired vertical subglottic stenosis.
History of the Procedure
Early in the 20th century, acquired subglottic stenosis (SGS) was usually related to trauma or infection from syphilis,
tuberculosis, typhoid fever, or diphtheria. Also, children often had tracheotomies placed that caused laryngealstenosis. In this era, attempted laryngeal dilation failed as a treatment for subglottic stenosis (SGS).
Acquired subglottic stenosis (SGS) occurred increasingly in the late 1960s through the 1970s, after McDonald and
Stocks (in 1965) introduced long-term intubation as a treatment method for neonates in need of prolonged ventilation
for airway support. The increased incidence of subglottic stenosis (SGS) focused new attention on the pediatric
larynx, and airway reconstruction and expansion techniques were developed.
Surgery without cartilage expansion
In 1971, Rethi and Rhan described a procedure for vertical division of the posterior lamina of the cricoid cartilage
with Aboulker stent placement. A metal tracheotomy tube was attached to the Aboulker stent with wires, and the
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anterior cartilaginous incision was closed. In 1974, Evanston and Todd described success with a castellated incision
of the anterior cricoid cartilage and upper trachea, which was sewn open, and a stent made of a rolled silicone sheet
was placed in it for 6 weeks. In 1980, Cotton and Seid described a procedure, in which tracheotomy is avoided,
called the anterior cricoid split (ACS). The procedure was designed for use in neonates (usually, those born
prematurely) with anterior glottic stenosis or SGS who had airway distress after extubation. The cricoid ring was
divided anteriorly and a laryngofissure was created in an attempt to expand the airway without a tracheotomy.
Holinger et al also described success with this procedure in 1987.
Surgery with cartilage-grafting reconstruction
In 1974, Fearon and Cotton described the successful use of cartilage grafts to enlarge the subglottic lumen in African
green monkeys and in children with severe laryngotracheal stenosis.[1]
All augmentation materials were evaluated,
including thyroid cartilage, septal cartilage, auricular cartilage, costal cartilage, hyoid bone, and sternocleidomastoid
myocutaneous flaps. After significant work, it appeared that costal cartilage grafts had the highest success rate.
In the 1980s, Cotton reported his experience with laryngeal expansion with cartilage grafting. His success rates
depended on degree of stenosis: More severe forms of stenosis required multiple surgical procedures. Cotton used
the Aboulker stent.
In 1991, Seid et al described a form of single-stage laryngotracheal reconstruction in which cartilage was placed
anteriorly to expand the subglottis and upper trachea to avoid a tracheotomy.[2]
In 1992, Cotton et al described a 4-quadrant cricoid split, along with anterior and posterior grafting. [3] In 1993, Zalzalreported 90% decannulation with any degree of subglottic stenosis (SGS) with his first surgical procedure.
[4]Zalzal
customized the reconstruction on an individual basis, and most patients received Aboulker stents for stabilization.
Cricotracheal resection
In 1993, Monnier described partial cricotracheal resection with primary anastomoses for severe SGS, since grade III
and grade IV SGS (ie, severe SGS) often requires multiple (3-4) surgical augmentations for decannulation. In 1997,
Cotton described his experience with the procedure, reporting a decannulation rate higher than 90% for primary and
rescue cricotracheal resection.
Problem
Subglottic stenosis (SGS) is narrowing of the subglottic lumen. Subglottic stenosis (SGS) can be acquired or
congenital. Acquired subglottic stenosis (SGS) is caused by either infection or trauma, as seen in the images below.
Congenital subglottic stenosis (SGS) has several abnormal shapes.
Grade III subglottic stenosis in an 18-year-old patient following a motor vehicle accident. The true vocal cords are seen in the
foreground. Subglottic stenosis is seen in the center of the picture.
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Granular subglottic stenosis in a 3-month-old infant that was born premature, weighing 800 g. The area is still granular followingcricoid split. This patient required tracheotomy and eventual reconstruction at age 3 years. True vocal cords are shown in theforeground (slightly blurry).
Intraoperative laryngeal view of the true vocal cords of a 9-year-old boy. Under the vocal cords, a subglottic stenosis can be seen.
This spiraling subglottic stenosis is not complete circumferentially. Laser therapy was the treatment choice and was successful
after 2 laser treatments.
Continued lasering of the subglottic stenosis. The reflected red light is the aiming beam for the CO2 laser.
Postoperative view. Some mild residual posterior subglottic stenosis remains, but the child is asymptomatic and the airway is
open overall.
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Preoperative view of a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Vocal cords are in the
foreground.
A close-up view.
Postoperative view. The patient had been intubated for 1 week and extubated for 1 week.
A subglottic view following dilation with an endotracheal tube to lyse the thin web of scar and a short course (5-day) treatment withoral steroids.
Postoperative view of a 4-month-old infant with subglottic stenosis following cricoid split. Notice very mild recurrence of scaring atthe site of previous scar. Overall, the airway is open and patent. The anterior superior area can be seen, with a small area of
fibrosis where the cricoid split previously healed.
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Preoperative subglottic view of a 2-year-old patient with congenital and acquired vertical subglottic stenosis.
Holinger evaluated 29 pathological specimens obtained in children with congenital cricoid anomalies. Half of these
children had an elliptical cricoid cartilage, as shown below, which Tucker first described in 1979.
Subglottic view of congenital elliptical subglottic stenosis.
Elliptical cricoid cartilage was the most commonly observed congenital abnormality. Other observed abnormalities
included a flattened anterior shape, a thickened anterior cricoid, and a submucosal posterior laryngeal cleft.
Epidemiology
Frequency
The frequency of congenital subglottic stenosis (SGS) is unknown.
The incidence of acquired subglottic stenosis (SGS) has greatly decreased over the past 40 years. In the late 1960s,when endotracheal intubation and long-term ventilation for premature infants began, the incidence of acquired
subglottic stenosis (SGS) was as high as 24% in patients requiring such care. In the 1970s and 1980s, estimates of
the incidence of subglottic stenosis (SGS) were 1-8%.
In 1998, Choi reported that the incidence of subglottic stenosis (SGS) had remained constant at the Children's
National Medical Center in Washington, DC; it was approximately 1-2% in children who had been treated in the
neonatal ICU.[5]
Walner recently reported that, among 504 neonates who were admitted to the level III ICU at the
University of Chicago in 1997, 281 were intubated for an average of 11 days, and in no patient did subglottic stenosis
(SGS) develop over a 3-year period. In 1996, a report from France also described no incidence of subglottic stenosis
(SGS) in the neonatal population who underwent intubation with very small endotracheal tubes (ie, 2.5-mm internal
diameter) in attempts to prevent trauma to the airway.
Etiology
The cause of congenital subglottic stenosis (SGS) is in utero malformation of the cricoid cartilage.
The etiology of acquired subglottic stenosis (SGS) is related to trauma of the subglottic mucosa. Injury can be
caused by infection or mechanical trauma, usually from endotracheal intubation but also from blunt, penetrating, or
other trauma. Historically, acquired subglottic stenosis (SGS) has been related to infections such as tuberculosis and
diphtheria. Over the past 40 years, the condition has typically been related to mechanical trauma.
Factors implicated in the development of subglottic stenosis (SGS) include the size of the endotracheal tube relative
to the child's larynx, the duration of intubation, the motion of the tube, and repeated intubations. Additional factors
that affect wound healing include systemic illness, malnutrition, anemia, and hypoxia. Local bacterial infection may
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play an important roll in the development of subglottic stenosis (SGS). Gastroesophageal reflux (GER) may play an
adjuvant role in the development of subglottic stenosis (SGS) because it causes the subglottis to be continually
bathed in acid, which irritates and inflames the area and prevents it from healing correctly. A systemic or
gastrointestinal allergy may cause the airway to be more reactive, creating a greater chance of developing stenosis.
Pathophysiology
Acquired subglottic stenosis (SGS) is often caused by endotracheal intubation. Mechanical trauma from an
endotracheal tube, as it passes through or remains for long periods in the narrowed neonatal and subglottic airway,
can lead to mucosal edema and hyperemia. These conditions then can progress to pressure necrosis of the mucosa.These changes have been observed within a few hours of intubation and may progress to expose the perichondrium
of the cricoid cartilage. Infection of the perichondrium can result in a subglottic scar. This series of events can be
hastened if an oversized endotracheal tube is used. Always check for an air leak after placing an endotracheal tube
because of the risk of necrosis of the mucosa, even in short surgical procedures. This practice is common among
anesthesiologists. Usually, the pressure of the air leak should be less than 20 cm of water, so that no additional
pressure necrosis occurs in the mucosa of the subglottis.
Presentation
History
Children with subglottic stenosis (SGS) have an airway obstruction that may manifest in several ways. In neonates,subglottic stenosis (SGS) may manifest as stridor and obstructive breathing after extubation that requires
reintubation. At birth, intubation in most full-term neonates should be performed with a 3.5-mm pediatric
endotracheal tube. If a smaller-than-appropriate endotracheal tube must be used, narrowing of the airway may be
present, which could suggest subglottic stenosis (SGS).
The stridor in subglottic stenosis (SGS) is usually biphasic. Biphasic stridor can be associated with glottic, subglottic,
and upper tracheal lesions. Inspiratory stridor usually is associated with supraglottic lesions; expiratory stridor usually
is associated with tracheal, bronchial, or pulmonary lesions.
The level of airway obstruction varies depending on the type or degree of subglottic stenosis (SGS). In mild
subglottic stenosis (SGS), only exercise-induced stridor or obstruction may be present. In severe subglottic stenosis
(SGS), complete airway obstruction may be present and may require immediate surgical intervention.
Depending on the severity, subglottic stenosis (SGS) can cause patients to have decreased subglottic pressure and
a hoarse or a weak voice. Hoarseness or vocal weakness also can be associated with glottic stenosis and vocal cord
paresis or paralysis.
Always ask about a history of recurrent croup. A child with an otherwise adequate but marginal airway can become
symptomatic with the development of mucosal edema associated with a routine viral upper respiratory infection
(URI). Children with these conditions may have subglottic narrowing and an evaluation of the airway is appropriate.
Always assess the history of GER disease (GERD). If present, always evaluate GERD prior to surgical intervention.
A child who eventually has a diagnosis of subglottic stenosis (SGS) often has a history of either laryngotracheal
trauma or intubation and ventilation. Frequently, these patients were born prematurely, have bronchopulmonary
dysplasia, and may require oxygen administration. The degree of pulmonary disease and the amount of oxygen the
child requires may affect the ability to perform decannulation. Prior to surgical intervention, the child should not
require a substantial oxygen supplementation.
Physical examination
The physical examination varies depending on the degree of subglottic stenosis (SGS) present. Auscultate the
child's lung fields and neck to assess any symptoms of airway obstruction and to evaluate pulmonary function.
Completely evaluate the head and neck, and identify associated facial abnormalities such as cleft palate, choanal
atresia, retrognathia, and facial deformities. Evaluate the child's initial overall appearance, and ask the following
questions:
Is the child comfortable?
Does the child have difficulty breathing?
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Does the child have difficulty breathing when emotionally upset?
Does the child have any suprasternal, substernal, or intercostal retractions?
Does the child have any nasal flaring?
Is the voice normal? Is it weak? Is the voice breathy?
Does the child have stridor? If so, what is the nature of the stridor (ie, inspiratory, expiratory, or biphasic)?
What is the child's neurologic status?
Does the child have a tracheotomy? Can the patient occlude the tracheotomy and still breathe without
laboring?
Indications
Staging
Surgical reconstruction is performed on the basis of the symptoms, regardless of SGS grade. Children with grade I
and mild grade II subglottic stenosis (SGS) often do not require surgical intervention.
Myers and Cotton devised a classification scheme for grading circumferential subglottic stenosis from I-IV, which is
established endoscopically and by using noncuffed pediatric endotracheal tubes of various sizes and sizing the
airway. The scale describes stenosis as a percent of area that is obstructed.
The system contains 4 grades, as follows:
Grade I - Obstruction of 0-50% of the lumen obstructionGrade II - Obstruction of 51-70% of the lumen
Grade III - Obstruction of 71-99% of the lumen
Grade IV - Obstruction of 100% of the lumen (ie, no detectable lumen)
The percentage of stenosis is evaluated by using endotracheal tubes of different sizes. The largest endotracheal
tube that can be placed with an air leak less than 20 cm of water pressure is recorded and evaluated against a scale
that has previously been constructed by Myers and Cotton, as depicted below.
Granulation tissue (superior center portion of the picture) that occurred at the graft site of a laryngotracheal reconstruction
performed with an anterior graft.
This grading system applies mainly to circumferential stenosis and does not apply to other types of subglottic
stenosis (SGS) or combined stenoses, although it can be used to obtain a rough estimate. Typically, children with
grade I, as shown in the image below, or mild grade II stenosis do not require surgical intervention. Children withthese conditions may have intermittent airway symptoms, especially when infection or inflammation causes mucosal
edema.
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Subglottic view of very mild congenital subglottic stenosis. Laterally, the area looks only slightly narrow. When endotracheal tubes
were used to determine its size, it was found to be 30% narrowed.
Indications
Surgical intervention may be avoided if periods of airway obstruction are rare and can be treated on an inpatient or
outpatient basis with anti-inflammatory and vasoconstrictive agents, such as oral, intravenous, or inhaled steroids
and inhaled epinephrine (racemic treatment). If children with these conditions continue to have intermittent or
persistent stridor and airway obstructive symptoms when they are well, or if they frequently become ill, surgical
intervention may be necessary.
Development of upper respiratory symptoms during routine infections can indicate whether a child with subglottic
stenosis (SGS) requires surgical reconstruction. Viral infections of the upper respiratory tract can create swelling in
any area of the respiratory epithelium from the tip of the nose to the lungs. If a child with subglottic stenosis (SGS)
has a cold and/or bronchitis but no significant symptoms of stridor or upper airway obstruction, the airway may be
large enough to tolerate stress, and reconstruction may not be needed. A history of recurrent croup suggests
subglottic stenosis (SGS).
Occasionally, older children have exercised-induced airway obstruction. At evaluation, these children may have
grade I or grade II subglottic stenosis (SGS). Expansion of the airway with cartilage augmentation may allow them to
lead a healthy and active lifestyle.
Children with grade III or grade IV subglottic stenosis (SGS) need one or more of the forms of surgical treatment
discussed in Surgical therapy.
Although croup, bacterial infection, GERD, and bronchopulmonary dysplasia may occur or be involved in the
development of subglottic stenosis (SGS), a history of prolonged endotracheal tube intubation is the most common
factor seen in patients with subglottic stenosis (SGS) that requires surgical correction.
Relevant Anatomy
The subglottis is defined as the area of the larynx housed by the cricoid cartilage that extends from 5 mm beneath
the true vocal cords to the inferior aspect of the cricoid ring, depicted in the image below. Because of the proximity
and close relationship of the subglottis to the glottic larynx, glottic stenosis often can be present with subglottic
stenosis (SGS). When SGS is corrected surgically, good voice quality can be preserved by not violating the true
vocal cords if they are uninvolved in the disease process.
Intraoperative endoscopic view of a normal subglottis
When creating the entry incision into the airway in an isolated subglottic stenosis (SGS), divide the cricoid cartilage,
upper 2 tracheal rings, and the inferior third to half of the laryngeal cartilage in the midline; avoid dividing the anterior
commissure. However, if the disease dictates or if exposure for repair cannot be obtained without dividing the
anterior commissure, carefully perform the procedure. Endoscopic guidance can help in preventing injury to the
glottic larynx.
If a laryngofissure is required for glottic stenosis or to gain access to the posterior aspect of the stenosis for suturing
of the posterior graft, care must be taken to identify the anterior commissure and correctly put it back into place.
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Once the laryngofissure is created in the midline, immediately suture the anterior aspect of the true vocal chords
near the anterior commissure to the laryngeal cartilage with a 6-0 monofilament suture such as polydioxanone (PDS)
or Monocryl. This procedure helps prevent anterior commissure from becoming blunted and helps mark
approximately where it should be once the laryngofissure is closed.
When dividing the posterior cricoid lumen, note that the esophagus is immediately adjacent and posterior to it. Take
care to avoid injuring the esophagus when completely dividing the posterior cricoid lamina during cartilage
augmentation.
The recurrent laryngeal nerves enter the larynx in the posterior lateral portion of the cricoid ring. When surgery is
performed in the midline, the recurrent laryngeal nerves should be far enough away from an anterior division toprevent injury. Any surgical procedure in which the lateral cricoid is divided could jeopardize the laryngeal nerve and
result in paresis or paralysis of the true vocal cords. In the cricotracheal resection procedure, no attempt is made to
identify the recurrent laryngeal nerves because of dense scarring. This lack of identification has resulted in some
reported cases of paresis of the true vocal cord.
Contraindications
No specific absolute contraindications to the laryngotracheal reconstruction procedure exist. However, if general
anesthesia is absolutely contraindicated, surgical correction of subglottic stenosis (SGS) cannot be performed.
A relative contraindication to reconstruction of a narrow subglottis is present in children who have a tracheotomy and
subglottic stenosis (SGS) but need a tracheotomy for other purposes (eg, access for suctioning secretions caused bychronic aspiration) or in those who have airway collapse or obstruction in the nasal cavity, nasopharynx, oral cavity,
oropharynx, supraglottic larynx, or trachea that cannot be repaired. However, if severe or complete laryngeal
obstruction exists and if the child might be able to vocalize if the airway were surgically corrected, reconstruction may
be beneficial, despite the need to maintain the tracheotomy tube. Severe GER is another relative contraindication.
Once GER is treated successfully (medically or surgically) or resolves on its own, reconstruction can be considered.
An additional relative contraindication to airway reconstruction is pulmonary or neurological function that is
inadequate to withstand tracheotomy decannulation.
Regardless of the cause of subglottic stenosis (SGS), it is usually best to delay reconstructive efforts in children who
have reactive or granular airways, shown below, until the reactive nature of the patient's condition subsides.
Granular subglottic stenosis in a 3-month-old infant that was born premature, weighing 800 g. The area is still granular followingcricoid split. This patient required tracheotomy and eventual reconstruction at age 3 years. True vocal cords are shown in the
foreground (slightly blurry).
Contributor Information and DisclosuresAuthor
John E McClay, MD Associate Professor of Pediatric Otolaryngology, Department of Otolaryngology-Head and
Neck Surgery, Children's Hospital of Dallas, University of Texas Southwestern Medical School
John E McClay, MD is a member of the following medical societies: American Academy of Otolaryngic Allergy,
American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, and American
Medical Association
Disclosure: Nothing to disclose.
Specialty Editor Board
Russell A Faust, MD, PhD Consulting Staff, Department of Otolaryngology, Columbus Children's Hospital
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Russell A Faust, MD, PhD is a member of the following medical societies: American Academy of
Otolaryngology-Head and Neck Surgery, American College of Legal Medicine, American Laryngological
Rhinological and Otological Society, American Rhinologic Society, American Society for Head and Neck Surgery,
and American Society of Law, Medicine & Ethics
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Gregory C Allen, MD Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, University of
Colorado School of Medicine
Gregory C Allen, MD is a member of the following medical societies: American Academy of Otolaryngology-Head
and Neck Surgery, American Academy of Pediatrics, American Cleft Palate/Craniofacial Association, American
College of Surgeons, American Laryngological Rhinological and Otological Society, American Medical
Association, Christian Medical & Dental Society, and Colorado Medical Society
Disclosure: Nothing to disclose.
Christopher L Slack, MD Private Practice in Otolaryngology and Facial Plastic Surgery, Associated CoastalENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy
of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and
American Medical Association
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA Professor, Department of Otolaryngology-Head and Neck Surgery, University of
Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic
and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head
and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis
Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra
Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy
Ownership interest Management position; Cerescan Imaging Honoraria Consulting; GYRUS ACMI Honoraria
Consulting
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