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the ppt includes the anatomy of larynx, the physiology of sound production and pathology of vocal cords explaining the myoelastic aerodynamic theory and bernoulli effect in phonation
This is a presentation I used for my seminar on 'Phonosurgery' on 4th November, 2015. I hope they are useful to you. Constructive as well as Destructive criticism welcomed.
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The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
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http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
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This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
2. CLASSIFICATION
1..CARTILAGINOUS ANOMALIES-
A. SUPRA GLOTTIC ANOMALIES
- Laryngomalacia
- Epiglottic anomalies (absent or bifid )
B. GLOTTIC ANOMALIES
-Atresia
- Laryngeal cleft
C. SUBGLOTTIC ANOMALIES
- Stenosis
- Atresia
3. 2. SOFT TISSUE ANOMALIES
A. Cyst and Laryngoceles
B. Tracheoesophageal fistula
C. Webs and Stenosis
D. Reduplication
3. COMBINED ANOMALIES
A. Atresia
4. NEUROLOGICALANOMALIES
A. Vocal cord palsy
5. HAMARTOMATOUS ANOMALIES
A. Haemangioma
B. Lymphangioma
4. LARYNGOMALACIA
Also known as Congenital laryngeal stridor.
Most common cause of stridor in infants.
Occurence ratio- M:F -2:1.
Theories of Causation –
-Congenital malformation of the larynx associated with abnormal f
flaccidity of laryngeal cartilage resulting in stridor.
- Delayed development of neuromuscular control leading to laryngeal hypotonia.
- Anatomical abnormality .
5.
6. Pathophysiology of Laryngomalacia
Softness or lack of consistency of laryngeal
tissue
Hypocellularity of laryngeal tissue
Wrinkled loose mucosa
Ary epiglottic fold is short antero posteriorly
80% of cases are associated with GERD
7.
8. Clinical features
Inspiratory stridor, high pitch type within few
days of birth, more in 8months (9-12 months)
Cry is clear, strong and normal
Cyanotic attacks are uncommon
Airway obstructive symptoms
15. BIFID EPIGLOTTIS
Congenital bifid epiglottis is a rare congenital laryngeal anomaly
Epiglottis fails to fuse in midline resulting in cleft extending down to its
tubercle
Presents as laryngomalacia with inspiratory stridor and airway obstruction.
16. Bifid epiglottis may be associated with congenital syndromes most commonly
Pallister-Hall syndrome.
Patients with bifid epiglottis should undergo an endocrine evaluation because of
the possibility of associated hypothyroidism or hypothalamic abnormalities.
17. Investigations
Flexible endoscopy
Treatment
In cases of severe airway obstruction, surgical management is necessary.
Endoscopic removal of the malacic portion of the bifid epiglottis
CO2 laser to relieve the airway obstruction.
18. LARYNGEAL ATRESIA
Rare lesion.
Arise from premature arrest of normal
epithetial ingrowth into the larynx.
Atresia occurs when laryngeal opening fails to
develop and obstruction is created at or near
the glottis.
Tracheoesophageal fistulae are frequently
associated with this condition and usually
arise at tracheal bifurcation.
19. Symptoms- child becomes markedly cyanotic when umbilical cord is clamped .
Child does not cry or manifest any stridor.
Investigation made before birth by ultrasonography by noting enlarged oedematous lungs, compressed
fetal heart, severe ascites and fetal hydrops.
Extracorporeal tracheostomy can be done during caesarean section .
20. LARYNGEAL CLEFT
Posterior laryngeal cleft or laryngotracheal esophageal cleft, is an uncommon congenital laryngeal
anomaly
Typically presents with aspiration, stridor, and weak cry at birth.
21. Posterior laryngeal cleft (PLC) may be an isolated laryngeal anomaly or associated with other
congenital anomalies.
Tracheoesophageal fistula
Esophageal atresia
Cleft lip and palate
Congenital heart defects (transposition of great vessels)
Gastrointestinal anomalies (imperforate anus, rectal stenosis, Meckel's diverticulum)
Genitourinary anomalies ( hypoplastic kidneys)
Subglottic stenosis
22. The embryologic defect that causes an abnormal opening in the posterior larynx
or posterior trachea results from a failure of fusion of the tracheoesophageal
septum and of the dorsal laminae of the cricoid cartilage
The failure of fusion may result in an abnormal communication limited just to the
larynx itself, or extending into the cervical and, possibly, thoracic trachea
23. Benjamin and Inglis classification
Type I Supraglottic, interarytenoid cleft
Type I1 Partial cricoid cleft
Type I11 Complete cricoid cleft with or without extension into part of trachea-
esophageal wall
Type IV Laryngotracheal esophageal cleft
26. Treatment
Type 1 : No surgical intervention
Type 2 : Repair endoscopically followed by NG feeds
Type 3 : Low tracheostomy and laryngofissure approach
Type 4 : Endotracheal intubation for 10 days
Short cleft : cervical approach
Long cleft : lateral cervical approach with tracheostomy or cervicothoracic
approach with medial sternotomy
27. SUBGLOTTIC STENOSIS
Narrowing of less than 4mm at the subglottic region
3rd most common congenital anomaly
More common in males
Subglottic stenosis may be associated with other congenital anomalies, such as
vocal cord paralysis or congenital syndromes, such as Down syndrome
40. Type A: In this type, there is Oesophagal Atresia and proximal and distal
segments of oesophagus are blind. There is no communication between trachea
and oesophagus. This type is present in 3-7 % of cases
Type B: In this type, Oesophagal Atresia is present and the blind proximal
segment of oesophagus connects with trachea by a fistula. The distal end of
oesophagus is blind. This type is present in 0.8 % cases.
Type C: In this type, Oesophagal Atresia is present. The proximal end of
oesophagus is a blind pouch and distal segment of oesophagus is connected by
fistula to trachea. This is the commonest type, present in about 87 % cases.
41. Type D: It is the rarest type that occurs in 0.7 % cases. In this type, both upper
and lower segments of oesophagus communicate with trachea.
Type E: In this type, oesophagus and trachea are normal and completely formed
but are connected by a fistula. This type is also known as ‘H’ type and is present
4.2% cases.
42. Clinical Features
Disorder is usually detected soon after birth when feeding is attempted on the
basis of following :
1. Violent response occurs on feeding
2.Infant coughs and chokes
3.Fluid returns through nose and mouth.
4.Cyanosis occur
5.The infant struggles
43. Excessive secretions coming out of nose and constant drooling of saliva.
Abdominal distension occurs in presence of type III, IV and V fistula.
Intermittent unexplained cyanosis and laryngospasm, caused by aspiration of
accumulated saliva in blind oesophageal pouch.
Pneumonia may occur due to overflow of milk and saliva from oesophagus
through fistula into the lungs
44. TEF may be suspected prenatally if
Ultrasound examination reveals polyhydramnios, absence of a fluid-filled stomach,
a small abdomen, lower-than expected fetal weight, and a distended esophageal
pouch.
45. TEF may be detected postnatally by
X-ray taken with radiopaque catheter placed in esophagus to check for obstruction;
standard chest X- ray shows a dilated air-filled upper esophageal pouch and can
demonstrate pneumonia.
Inability to pass a NG tube into stomach because it meets resistance
Bronchoscopy visualizes fistula between trachea and esophagus
46. The management of tracheaoesophageal fistula is mainly surgical. Surgical
intervention depends on the distance between proximal and distal pouch of
oesophagus, type of defect.
If distance between upper and lower oesophageal segments is less than 2.5 cm
and if the condition of infant is good, primary repair is done by division and
ligation of the fistula along with end-to-end anastomosis of proximal and distal
segments of oesophagus.
47. CONGENITAL VOCAL CORD PALSY
Third most common congenital laryngeal anomaly causing stridor.
Unilateral & Bilateral (1:1) .
50% are associated to other anomalies
Acquired paralysis
- 70% association to congenital neurologic abnormalities or neurosurgical
procedure.
-Unilateral are associated to cardiovascular anomalies (PDA) and left side is more
common.
48.
49. Symptoms –
Bilateral - High-pitched inspiratory stridor
- Inspiratory cry
-Paradoxical function (pressure changes)
-close during inspiration and open during expiration.
Unilateral – weak cry .
- Feeding difficulties secondary to laryngeal
penetration and aspiration.
50. Awake flexible fiberoptic laryngoscopy
Direct laryngoscopy
Imaging of head (MRI) and chest to evaluate for associated abnormalities
(Neurologic & CV)
51. Wait and watch
70% of idiopathic unilateral VC paralysis resolve spontaneously
Most within 6 month
Speech therapy
Rare surgical management
52. Bilateral VC Paralysis treatment
Tracheostomy may be necessary (50%)
Lateralizing one or both paralyzed vocal cords
Excisional procedure -Tissue removed from posterior glottis
Endoscopic technique with laser
More consistent results are achieved by external approach
53. LARYNGEAL WEBS
Uncommon
Failure of laryngeal recanalization
Most common site - glottic (75%)
Symptoms
Vocal dysfunction
Hoarseness
Aphonia
Airway obstruction (if severe)
Complete laryngeal atresia is incompatible with life and need emergency tracheostomy
54. Laryngeal Web Diagnosis
Flexible laryngoscopy
Direct Laryngoscopy
Airway films if subglottic or cricoid pathology are present
55. Treatment
Mild form requires no treatment.
Web is divided endoscopically along the margin of one vocal cord with a knife ,
scissors or laser.
56. LARYNGEAL HEMANGIOMA
Benign vascular malformations
Subglottic haemangiomas is most common neoplasm of infant airway.
Female predominance 2:1
Asymptomatic at birth
Stridor presents by 6 months (85%)
Associated cutaneous hemangioma (50%)
57. Rapid growth phase in the 1st year followed by slow resolution
Most have complete resolution by 5 years
30-70% mortality rate if untreated
Priority is to maintain the airway while minimizing potential long term sequelae
59. Treatment
Systemic steroids (principal)
Partial regression in most patients (82-97%)
Risk of growth retardation and increase susceptibility to infection
Risk is reduced by alternate-day dosing regimen in the smallest doses
Also intralesion corticosteroids has been employed with successful avoidance of
tracheotomy
Interferon alpha-2a
50% or greater regression of lesion in 73% of patients
It requires prolonged therapy, blocks various steps of angiogenesis
Side effects neuromuscular impairment, skin slough, fever and liver enzyme elevation
60. Treatment (contd)..
Tracheostomy
Bypass the obstructing lesion
Waiting for the expected involution
Risks of tracheostomy as well as delay in speech and language
Laser CO2 and KTP
associated with a significant risk of inducing subglottic stenosis in up to 20%
