Airway Pathology (not sleep) - Stridor, RRP, infections Flashcards

Question 1

Q

What is the rule for choosing appropriate pediatric ETT sizes?

Answer

A

ETT cuffed = (Age in years/4) + 4 (some say 3.5 for cuffed)
= Size of inner diameter of bronchoscopy (for ages 2-10 years)

Uncuffed = (Age + 16) / 4

Note:
- ETTs are measured and numbered by Inner diameter
- Estimate size using a child’s pinky finger (estimates size of subglottis, the narrowest part of child)
- For infants < 1 year of age, use 3.5mm inner diameter tube

Question 2

Q

What are the pediatric bronchoscope sizes based on age of child?
What is the smallest bronchoscope that will fit a peanut grasper?
How do you measure the outer diameter?

Answer

A

Measured by inner diameter
Estimate with ETT size calculation (want ~1-2mm smaller than airway diameter to be able to fit

Size, (inner diameter, outer diameter)

Premie = 2.5 (3.7)
Term = 3 (5.0)
6 months to 1 year = 3.5 (smallest size that will fit a peanut grasper) (5.7)
1-3 years = 3.7 (6.3)
2-5 years = 4 (6.7) or 5 (7.8)
5-10 years = 5 (7.8)
10+ years = 6 (8.2)

Outer diameter (and size of airway) = approximately ID + 1.5-2 (Vancouver is ID + 0.8)

Vancouver 472

Question 3

Q

What is the estimated endotracheal tube, tracheostomy tube, and ventilating bronchoscope sizing chart by age?

Answer

A

Premature:
- ETT: 2.5
- Tracheostomy: 2.5
- Bronchoscope: 2.5

0-6 months:
- ETT: 3
- Tracheostomy: 3
- Bronchoscope: 3

6-12 months:
- ETT: 3.5
- Tracheostomy: 3.5
- Bronchoscope: 3.5

1-2 years:
- ETT: 4
- Tracheostomy: 4
- Bronchoscope: 3.7

2-3 years:
- ETT: 4.5
- Tracheostomy: 4.5
- Bronchoscope: 4

3-4 years:
- ETT: 4.5
- Tracheostomy: 5
- Bronchoscope: 4.5

4-5 years:
- ETT: 5
- Tracheostomy: 5.5
- Bronchoscope: 5

Question 4

Q

What are the pediatric laryngoscope sizes?

Answer

A

0-6 months: 8
6-12 months: 9
1-5 years: 11
5-10 years: 13.5 (does not have side port for oxygen)
10+ years: As per adult

Question 5

Q

What are the pediatric esophagoscope sizes?

Answer

A

Approximately 1/2 laryngoscope size and round up to a whole number

0-6 months: 4
6-12 months: 5
1-5 years: 6
5-10 years: 7
10+ years: As per adult

Question 6

Q

What are the four methods of ventilating a pediatric patient during suspension laryngoscopy?

Answer

A

Spontaneous breathing
Intubation (± intermittent extubation)
Tracheostomy

Note: Cannot use jet ventilation in kids

Question 7

Q

Label the parts of a bronchoscope (Vancouver 471)

Answer

A

Ventilation holes
Prism for light source
Adaptor to connect the ventilation circuit
Locking mechanism to secure camera
Extension collar for use with endoscope
Endoscope
7Fr suction tubing

Question 8

Q

Regarding CHAOS syndrome, discuss:
1. What is it?
2. What is the pathophysiology
3. List some possible etiologies
3. What are the fetal features
4. What are some associations
5. How is it diagnosed?
5. What is the treatment

Answer

A

CHAOS = Congenital High Airway Obstruction Syndrome

PATHOPHYSIOLOGY:
1. Laryngeal/tracheal obstruction (partial or complete atresia)
2. Continually produced pulmonary secretions get trapped in lungs
3. Dilated fluid-filled lungs compress heart, push on diaphragm/abdomen

POSSIBLE ETIOLOGIES:
1. Complete laryngeal web / laryngeal atresia
2. Tracheal agenesis
3. Lymphangiomas (anterior compartment)
4. Teratomas (anterior compartment)

FETAL FEATURES:
1. Enlarged echogenic lungs
2. Compressed heart
3. Flattened or inverted diaphragm
4. Abdominal ascites
5. Polyhydramnios

DIAGNOSIS:
1. Prenatal: Fetal MRI
- Enlarged and echogenic lungs
- Inverted or flattened diaphragms
- Massive ascites
- Dilated fluid-filled lower airways (tracheobronchial tree)
- Fetal hydrops
- Polyhydramnios

ASSOCIATIONS:
- Fraser Syndrome

TREATMENT:
1. EXIT procedure

Question 9

Q

Define the EXIT procedure. How is it performed, describe the steps?

Answer

A

EXIT = Ex-utero intrapartum treatment procedure

Done for babies with airway compression upon delivery
- Partial delivery through a C-section but remain attached by their umbilical cord to the placenta
- Airway is then established via tracheostomy
- The umbilical cord is cut and clamped, then the infant is then fully delivered

Question 10

Q

Compare features of pediatric vs. adult upper airways

Answer

A

Pediatrics have:
1. Larger tongue
2. Relatively hypotonic/floppier tissues
3. Higher, more anterior larynx (at C2 vs. C6 in adults)
4. High, long epiglottis (touches soft palate - therefore infants are obligate nasal breathers)
5. Differently shaped epiglottis - longer, omega shaped
6. Large arytenoids (50% of larynx area vs. 25% in adults) –> obstruction vocal portion of cords
7. Funneled shaped larynx (vs. tube shape of adults)
8. Soft tracheal cartilages
9. Narrowest part of pediatric airway = cricoid cartilage/subglottis until ~8 years (vs. glottis in adults)

Question 11

Q

What are the age-related anatomical differences in the larynx between infants and adults?

Answer

A

SIZE:
1. Infant larynx 1/3 size of adult larynx
2. Infant VF 4-4.5mm at birth, up to 7-8mm length, adults 14-23mm
3. Half of VF is composed of the vocal process to the arytenoid in infants; vocal process in adults only occupies 1/4-1/3 of the total length of the true VF
4. Subglottis is narrowest part of the airway because of complete cricoid ring
5. Infant subglottis = 4.5-7mm (< 4mm = subglottic stenosis)

QUALITY:
1. Superficial, intermediate, and deep lamina propria of true vocal folds are not differentiated well in young children
2. Infant subglottis is loose tissue
3. Lots of submucosal glands in infant subglottis

LOCATION:
1. Pediatrics have higher and more anterior larynx (C2-4 vs. C5-6)
2. Superior border of the larynx is at the first cervical vertebrae (cricoid at 4th cervical vertebrae)
2. Hyoid overrides superior larynx in pediatrics
3. Thyroid notch is not palpable in kids
4. Epiglottis approximates the dorsal surface of soft palate and contributes to obligate nasal breathing in pediatrics
5. Larynx descends and cricoid rests at the level of the 6th cervical vertebrae (in adults)
6. Epiglottis is omega-shaped, narrower, softer, less stable base, more acute angle between the epiglottis and glottis (allows epiglottis to fall into laryngeal inlet), may contact soft palate
7. Angle of thyroid cartilage changes from 110-120 degrees to 90 degrees (in adolescent males). Adult females are more obtuse like in childhood

Question 12

Q

What is the physiologic role of the superior larynx in an infant?

Answer

A

Creates an overlap of the epiglottis and velum, increasing a patent nasopharyngeal airway
Ensures inspired air is humidified (via nose)
Enables simultaneous suckling and feeding in the infant

Question 13

Q

At what age does the cricoid no longer become the narrowest segment of the airway?

Answer

A

8 years old

Question 14

Q

Name 5 reasons why pediatric bronchoscopy is more difficult compared to adults?

Answer

A

Omega epiglottis
Oblique thyroid cartilage
Narrow subglottis
Large arytenoids
Smaller diameter

Question 15

Q

What are the different methods of pediatric voice assessment?

Answer

A

Audiotape and videotape recording (speech therapist)
Parent and child questionnaire (pVHI)
Fiberoptic laryngoscopy with videostroboscopy
Spectral voice analysis = multi-dimensional voice program (MDVP)

Question 16

Q

List a complete differential for infant stridor

Answer

A

A. CONGENITAL
1. Laryngomalacia
2. Laryngocele
3. Saccular cyst
4. Laryngeal web/atresia
5. Subglottic cyst
6. Subglottic stenosis
7. Tracheomalacia
8. Tracheal web/stenosis
9. Vascular anomalies
10. Complete tracheal rings
11. Thymic cyst

B. INFECTIOUS / INFLAMMATION
1. Retropharyngeal abscess
2. Epiglottitis
3. Angioedema
4. Viral laryngotracheobronchitis (croup)
5. Bacterial Tracheitis
6. GERD

C. NEOPLASMS
1. Vascular tumors - hemangiomas, vascular malformations
2. RRP
3. Thyroid tumors
4. Mediastinal tumors

D. TRAUMATIC
1. Birth trauma
2. Intubation trauma - cricoarytenoid dislocation

OTHER
1. Vocal cord immobility
2. Foreign body
3. Laryngeal fracture

Question 17

Q

What is the common location of stridor based on its pattern:
1. Inspiratory
2. Biphasic
3. Expiratory

Answer

A

Inspiratory = Dynamic supraglottis and glottis

Biphasic = Subglottis and cervical trachea

Expiratory = Fixed itnrathoracic trachea

Question 18

Q

What is the percentage of laryngeal anomalies with other airway anomaly?

Question 19

Q

What is the duration of obligate nasal breathing in an infant?

Answer

A

Begins at birth and lasts 6 weeks to 6 months

Question 20

Q

What are the pertinent points to ask on a pediatric stridor history?

Answer

A

Severity, parents subjective impression
Progression of obstruction over time
Eating and feeding difficulties
Cyanotic spells
Sleep disordered breathing
Prematurity
History of endotracheal intubation
Aspiration of foreign body
X-rays for specific abnormality

Question 21

Q

What are signs of upper airway obstruction?

Answer

A

Stridor - note the phase of respiratory cycle to help locate the etiology
Dyspnea, tachypnea
Tachycardia
Diaphoresis, circumoral pallor, anxiety/restlessness
Retractions - tracheal tug, suprasternal, intercostal, substernal
Flaring of nasal ala
Use of accesesory respiratory muscles
Cyanosis, in extreme cases
Respiratory arrest

Question 22

Q

What are the different types of airway imaging modalities?

Answer

A

Plain soft tissue films of the neck, AP (croup) + lateral (epiglottitis & RPA)
CXR AP + lateral (FB & tracheal stenosis); Inspiratory & expiratory chest films (FB)
Airway Fluoroscopy (dynamic, awake & sleep, best for OSA)
Barium swallow (vascular compression)
Spiral CT scan with apnea
MRI of the airway (intrathoracic vascular anomalies & masses)
Bronchogram (after MRI, if difficult tracheobronchial stenosis)
Laryngeal U/S

Question 23

Q

What are the 3 most common causes of congenital laryngeal stridor?

Answer

A

Laryngomalacia
Vocal fold paralysis
Stenosis (subglottic, tracheal)

Question 24

Q

What 4 pediatric airway abnormalities are improved in the prone position?

Answer

A

Laryngomalacia
Pierre-Robin Sequence
Vascular compression
Mediastinal mass

Question 25

Q

What is the differential diagnosis of congenital supraglottic abnormalities?

Answer

A

Laryngomalacia
Hemangioma
Lymphatic malformation
Laryngocele
Saccular cyst
Anomalous cuneiform cartilage (4th arch)
Bifid epiglottis
Supraglottic web

Question 26

Q

Regarding Laryngotracheobronchitis (croup), discuss:
1. What is the epidemiology?
2. What is the common organisms?
3. How is it transmitted? What is the incubation and infectious period?
4. What is the pathophysiology?
5. What is the clinical presentation?
6. How is it diagnosed?
7. What is the management?

Answer

A

CROUP = Viral Laryngotracheobronchitis
Most common cause of infectious infant stridor

EPIDEMIOLOGY:
1. 3-5% will have one episode during childhood (usually late autumn or winter)
2. 6 months - 3 years old
3. M > F (2:1)

ORGANISMS:
1. Parainfluenza virus Types 1-3 (most common 80%)
2. Influenza A + B
3. RSV
4. Adenovirus
5. Rare: measles, varicella, HSV, mycoplasma pneumoniae

TRANSMISSION:
1. Direct contact and exposure to nasopharyngeal secretions
2. Airborne droplets over short distances
- Incubation period: 2-6 days for parainfluenza virus type 1
- Infectious period: may shed x 2 weeks
- Symptomatic usually ~5 days - resolution after 2 days most common

PATHOPHYSIOLOGY:
- Viral infection of nasopharynx –> spreads to larynx and trachea (particularly VF and subglottis –> inflammatory response –> edema)
- Subglottis is limiited by complete cricoid ring, therefore swelling narrows lumen

CLINICAL PRESENTATION:
1. 1-2 days of viral prodrome URTI
2. Hallmark triad signs: Hoarseness, stridor (varying degrees of upper airway obstruction), expiratory component (seal-like barking cough)
3. Critical signs: Cyanosis, retractions, high resp rate, desaturations, biphasic stridor
4. 15% develop bacterial tracheitis superinfection: high fever, toxic
5. Complications: airway obstruction, pulmonary edema, pneumonia, bacterial tracheitis

DIAGNOSIS:
1. Clinical signs and symptoms
2. X-ray: “Steeple sign” of narrowed subglottis on AP X-ray - only 50% have this
3. FNL caution - may exacerbate airway symptoms

TREATMENT (self limited 3-5 days)
1. Home measures: reassurance, limit crying/agitation
2. Cool humidified air - moistens secretions, facilitates expectoration and prevents drying
3. Supplemental oxygen
4. Heliox (helium-oxygen) - reduces airway obstruction by promoting gas flow through partially obstructed airway
5. Saline nebs
6. Epi nebs / racemic epi - monitor for 3-4 hours post (rebound risk) - 0.5mL of 2.25% solution in 3cc NS
7. Steroid nebs
8. Systemic steroids 1-2mg/kg/day divided twice daily for PO; IV 0.15-0.6mg/kg for severe
9. Control airway if severe; ETT: use 1/2-1 size smaller tube than usual; if no air leak after 5-7 days, should inspect airway w/ endoscopy
11. Suspect bacterial superinfection if not resolving/worsening/toxic

INDICATIONS FOR ADMISSION:
1. Initial therapy is ineffective
2. Severe symptoms (e.g. decreased LOC, increased WOB, infants < 6 months)
3. Social circumstances raise concerns about follow up and appropriate access to care

Question 27

Q

What should you investigate for patients with recurrent croup?

Answer

A

Bronchoscopy r/o subglottic stenosis

Question 28

Q

What are the features of spasmodic croup?

Answer

A

Non-infective barky ough
1-3 year olds
Normal during the day, worse at night ± stridor

Question 29

Q

How do you differentiate subglottic stenosis from subglottic hemangioma?

Answer

A

Clinical: Palpate in OR - hemangioma is compressible

Imaging: MRA

Question 30

Q

Regarding subglottic hemangiomas, discuss:

What is the clinical presentation?
What is the typical location?
How is it typically diagnosed?
Treatment options?

Answer

A

CLINICAL PRESENTATION:
1. Often very similar to laryngomalacia presentation
2. Stridor/symptom onset ~6-8 weeks of age, worsen throughout first year of life

TYPICAL LOCATION:
Left posterolateral subglottis

DIAGNOSIS:
1. FNL = May see subglottic lesion (but must distinguish and rule out SGS)
2. OR = palpate (compressible vs. SGS which is not
3. Imaging: MRA

TREATMENT OPTIONS:
A. Medical
1. Propranolol
2. Steroids
3. PPI
4. Vincristine
5. Interferon-alpha

B. Surgical (if very large or failing medical treatment)
1. Laser not recommended (risk of deep scarring)
2. Tracheostomy
3. Anterior laryngofissure, lift mucosal flap, dissect out hemagnioma with bipolar, replace flap - for circumferential or bilateral hemangiomas

Question 31

Q

Regarding bacterial tracheitis, discuss:
1. Common causes
2. Epidemiology
3. Causative organisms
4. Pathophysiology
5. Clinical presentation
6. Diagnosis
7. Treatment and possible complications

Answer

A

COMMON CAUSE: Complication or progression of croup - 15%

EPIDEMIOLOGY:
1. Rare
2. Similar age group & timing to croup

ORGANISMS:
1. Strep
2. Staph (possible MRSA - should treat with Vanco)
3. M. Catarrhalis
4. H. flu

PATHOPHYSIOLOGY:
1. Starts as croup
2. Edema of VC and subglottis
3. Eventually becomes diffuse mucosal ulceration, pseudomembrane formation –> sloughs into trachea (worsening obstruction) –> purulent exudate throughout tracheobronchial tree

CLINICAL PRESENTATION:
1. Croup prodrome for several days, then rapid onset of tracheitis
2. Rapid onset (hours) –> severe respiratory distress, high fever
3. NO drooling or sore throat (compared to epiglottitis)
4. 50% develop concomitant pneumonia
Suspicion raised for non-resolving croup symptoms to standard croup treatment

DIAGNOSIS
1. Clinical diagnosis
2. X-ray: Obscured appearing tracheal airway on latera caused by sloughed mucosa. Typically normal epiglottis (Figure 201.10 Cummings Chapter 201). Possible steeple sign
3. Endoscopy in OR

TREATMENT:
1. Laryngoscopy/Bronch in OR - suck out exudates/pseudomembranes, get cultures
2. Control Airway
- Intubate in OR (50-90% require intubation)
- Extubate when afebrile, ETT cuff leak)
3. Antibiotics x 14 days: Vancomycin/Ceftriaxone
- Step down to PO once extubated (afebrile, cuff leak, decreased secretions) and cultures known

Complications (possible): Pneumonia

Question 32

Q

Regarding epiglottitis/supraglottitis, discuss:
1. What is it?
2. Epidemiology
3. Causative organisms
4. Transmission
5. Clinical presentation
6. Diagnosis
7. Treatment

Answer

A

DEFINITION:
- Cellulitiis of the supraglottic structures associated with profound edema, most noticeably of the epiglottis
- As epiglottis enlarged, it curls posteriorly and inferiorly, limiting patency and ease of airway visualization
- Additional mucous can easily lead to complete airway obstruction following this partial occlusion

EPIDEMIOLOGY:
- More rare in H. Flu vaccinated kids
- More common in adults or older kids
- May still occur if immunocompromised (failure to respond to vaccine), HIV+
- Atypical cases seen in Kawasaki disease and posttransplant lymphoprolifierative disorders

ORGANISMS:
1. Invasive H. influenza
2. Strep pneumoniae, GAS, staph, and other H. flu serotypes now more common since vaccine for H. flu introduced

TRANSMISSION:
1. Droplet, contact, airborne, blood-borne
2. Incubation 3 days, symptomatic 3 days, infectious 3 days

CLINICAL PRESENTATION:
1. Rapid onset and progressive over hours: Dysphagia, Drooling, Respiratory distress
2. Toxic and anxious appearing, High fever
4. Shallow respiration, inspiratory stridor, retractions
5. Throat pain –> speech limited because of pain
6. Critical airway signs: Inspiratory stridor, drooliing, tripoding, shallow rapid respirations, retractions, fever, toxic
7. Sudden laryngospasm with aspiration of secretions –> risk of respiratory arrest

DIAGNOSIS:
1. Clinical signs
2. Lateral X-ray (if stable): “Thumbprint sign” of thickened epiglottis
3. FNL (if stable - do NOT irritate toxic child, can trigger respiratory arrest) - thick beefy red epiglottis with exudates

TREATMENT:
1. Keep child calm, minimal intervention/exam
2. Avoid triggering laryngospasm
3. Secure airway
4. Emergency intubation in OR
5. Tracheostomy if unable to intubate
6. Edema usually subsides after 48 hours; extubate when afebriile, cuff leak
7. Antibiotics: 10 day course - broad spectrum with second or third-generation cephalosporin
- IV Ceftriaxone / Clindamycin
- Step down to PO once extubated
8. Steroids debated

COMPLICATIONS:
1. Epiglottic abscess (25%)
2. Bacteremia (90-95%)
3. Pneumonia
4. Cervical adenitis
5. Infectious complications: meningitis, pericarditis, septic arthritis, otitis media
6. Noninfections complications: hypoxia, airway obstruction, post-obstructive pulmonary edema

Question 33

Q

What is a non-infectious differential for supraglottitis/epiglottitis?

Answer

A

Chemical epiglottitis
Inhalational/thermal injury
Angioedema/allergy
Trauma
Sarcoid

Question 34

Q

What is the differential for epiglottic enlargment other than epiglottitis on lateral X-ray?

Answer

A

Angioneurotic edema
Allergic reaction
Trauma
Candida infection
AE fold cyst
Sarcoid
Corrosive ingestion
Lymphovascular malformation

Question 35

Q

When do patients get the Hib vaccine and what is its effectiveness?

Answer

A

2, 4, 6 months
Booster 12 to 15 months
≥ 95% effectiveness

Question 36

Q

Compare and contrast:
1. Laryngotracheitis (viral croup)
2. Supraglottitis
3. Bacterial tracheitis
4. Retropharyngeal abscess

With respect to the following:
1. Age
2. Onset
3. Prodrome
4. Fever
5. Hoarseness/Barky cough
6. Dysphagia
7. Toxic appearance
8. Radiographs

Answer

A

CROUP:
1. Age - 6mo-3year
2. Onset - Slow
3. Prodrome - URTI symptoms
4. Fever - Variable or none
5. Hoarseness/Barky cough - Yes
6. Dysphagia - No
7. Toxic appearance - No
8. Radiographs - Subglottic narrowing (steeple sign)

SUPRAGLOTTITIS:
1. Age - 1-8year
2. Onset - Rapid
3. Prodrome - None or mild URTI
4. Fever - High
5. Hoarseness/Barky cough - No
6. Dysphagia - Yes
7. Toxic appearance - Yes
8. Radiographs - Rounded, enlarged epiglottitis

BACTERIAL TRACHEITIS:
1. Age - 6 mo- 8 years
2. Onset - Rapid
3. Prodrome - URTI symptoms
4. Fever - High
5. Hoarseness/Barky cough - Yes
6. Dysphagia - Yes
7. Toxic appearance - Yes
8. Radiographs - Subglottic narrowing; diffuse haziness; tracheal wall irregularities

RETROPHARYNGEAL ABSCESS:
1. Age - 1-5years
2. Onset - Slow
3. Prodrome - URTI symptoms
4. Fever - Usually high
5. Hoarseness/Barky cough - No
6. Dysphagia - Yes
7. Toxic appearance - Variable
8. Radiographs - Widened prevertebral space

Question 37

Q

Discuss the Canadian Pediatric Vaccination Schedule

Answer

A

2 + 4 months:
- Diphtheria
- Pertussis
- Tetanus
- Polio
- H Flu
- Pneumococcal
- Rotavirus

6 months:
- Diphtheria
- Pertussis
- Tetanus
- Polio
- H Flu

1 year:
- Pneumococcal
- Meningococcal
- Measles
- Mumps
- Rubella

15 months:
- Varicella

18 months:
- Diphtheria
- Pertussis
- Tetanus
- Polio
- H Flu

4-6 years:
- Diphtheria
- Pertussis
- Tetanus
- Polio
- Measles
- Mumps
- Rubella
- Varicella

Grade 7:
- Meningococcal
- Hepatitis B

Grade 8:
- HPV

14-16 years:
- Diphtheria
- Pertussis
- Tetanus

Influenza: every autumn

Kevan Peds Question 108##

Question 38

Q

Regarding retropharyngeal abscess, discuss:

Causes. Where is the retropharyngeal space?
Epidemiology
Organisms
Clinical presentation
Diiagnosis
Treatment
RIsks/Complications

Answer

A

CAUSE:
1. Results from suppuration of retropharyngeal lymph nodes in patients with URTI
2. Kids: Primary infection of retropharyngeal nodes (Rouviere’s nodes) - disappears by 5 years
3. May be due to perforation of pharynx or upper esophagus by a foreign body
4. Adults: Secondary spread from infection of adjacent deep neck spaces

WHERE IS THE RETROPHARYNGEAL SPACE?
- Posterior to the larynx between the middle and deep layers of the deep cervical fascia
- Extends from base of the skull to the mediastinum

EPIDEMIOLOGY:
1. Rare, similar age group at timing to croup (6mos - 3 years)

ORGANISMS:
1. Aerobies (from nasopharynx)
- GAbhS
- Staph (possible MRSA)
- H flu
2. Anaerobies (from mouth)
- Bacteroides
- Peptostreptococcus
- Fusobacterium

CLINICAL PRESENTATION:
1. Progressive worsening sore throat, dysphagia, drooling, stridor
2. Neck stiffness, torticollis, possible neck mass

DIAGNOSTIC FINDINGS:
1. Clinical signs: May have lateral neck/post-oropharyngeal budge
2. Lateral Neck x-ray (must be extension and inspiratory x-ray, otherwise can be false positive)
- Soft tissue at any C-level > 1/2x the width of its vertebral body is 90% sensitive
- Soft tissue at C2 = > 7mm (all ages)
- Soft tissue at C6 = > 14mm (kids) and > 22mm (adults)
- Loss of lordosis
3. Consider CT to r/o abscess
4. MRI - hypointense on T1, hyperintense on T2

TREATMENT:
1. Control airway if concerned
- Intubate; extubate when afebrile, ETT cuff leak
2. Antibiotics x 14 days
- IV Clindamycin or Ceftriaxone (include anaerobic coverage) + Flagyl
- Step down to PO once extubated and cultures known
3. Surgical drainage of abscess
- Intubate, then transoral I&D in OR
- If mediastinal extent is noted external approach is favoured

RISKS/COMPLICATIONS:
1. Airway obstruction
2. Spontaneous abscess rupture –> aspiration
3. Spread to adjacent spaces –> mediastinitis
4. Pneumonia/chest empyema
5. IJV thrombosis
6. Carotid erosion
7. Atlantoaxial subluxation
8. Sepsis

Question 39

Q

Regarding Diphtheria-associated pharyngitis, discuss:
1. Definition
2. Incidence/epidemiology
3. Organism
4. Pathophysiology
5. Transmission
6. Clinical presentation
7. Diagnosis
8. Treatment
9. Possible complications

Answer

A

DEFINITION:
- Complication/progression of croup (15%)
- Corynebacterium diphtheriae infection that causes an early exudative pharyngotonsillitis with a thick pharyngeal membrane, that produces a lethal exotoxin that can damage distant organ cells

EPIDEMIOLOGY:
1. Rare since vaccine
2. Can occur in immunocompromised patients
3. Diphtheria titres drop with age - 10-year booster recommneded for adults, especially if going to endemic areas (e.g. Africa, India)

ORGANISM:
1. Corynebacterium diphtheriae (gram-positive pleomorphic aerobic bacillus)
- “Chinese character” appearance on Gram stain
- Best identified by culture on tellurite media

PATHOPHYSIOLOGY:
1. Infections nasopharynx/oropharynx/larynx
2. Toxin mediated tissue necrosis
3. Thick, fibrinous pseudomembrane formation –> can slough and obstruct airway

TRANSMISSION:
1. Droplet, airborne, contact
2. Incubation 2 days, symptomatic 10 days, infectious 14 days

CLINICAL PRESENTATION:
- Croup-like prodrome x 2 days (stridor, hoarseness, barky cough)
- Sore throat, dysphagia
- Thick Pseudomembrane on tonsils/oropharynx –> risk airway obstruction
- “Bull neck” of cervical LN enlargement –> can cause external compression
- Systemic infection

DIAGNOSIS:
1. Clinical signs/symptoms
2. Culture of pseudomembrane

TREATMENT:
1. Secure airway
- Do not intubate outside of controlled circumstance (given risk of membrane sloughing into airway)
- Intubate/tracheostomy in OR
2. Anti-toxin (prevent further systemic damage)
- Does not neutralize toxin alerady bound to tissues
- Ideally within 28 hours of onset
3. Antibiotics (eradicate bug)
- IV Erythromycin and Flagyl, Penicillin G,
- Booster vaccine one resolved
4. Serial ECGs to watch for myocarditis (up to 2 weeks post-infection)
5. Successful eradication = 2 negative cultures after treatment

COMPLICATIONS:
1. Myocarditis –> arrhythmias
2. Neurologic manifestations –> peripheral neuritis –> paralysis
3. Airway obstruction
4. Acute TUbular Necrosis (kidney injury)
5. Thrombocytopenia

https://upload.wikimedia.org/wikipedia/commons/thumb/4/47/Dirty_white_pseudomembrane_classically_seen_in_diphtheria_2013-07-06_11-07.jpg/1024px-Dirty_white_pseudomembrane_classically_seen_in_diphtheria_2013-07-06_11-07.jpg

Question 40

Q

What are the complications of EBV (mononucleosis) infection?

Answer

A

Airway obstruction (from tonsillar enlargement)
Splenomegaly/rupture (avoid contact sports x 6 months)
Hepatitis
CNS: meningitis, encephalitis, transverse myelitis
Guillain-Barre, cranial neuropathies (esp. CN7)
Hemolytic anemia
Myocarditis

Question 41

Q

How is HSV pharyngitis diagnosed?

Answer

A

Culture from swab of ulcer demonstrating multinucleated cells seen on Tzanck smear

Kevan Gen #55

Question 42

Q

Compare and contrast the following pharyngitis presentations:
1. Viral Pharyngitis
2. Infectious mononucleosis
3. Group A Strep
4. Diphtheria

with respect to the following categories:
1. Risk factors
2. Onset (rapid vs. slow)
3. Associated symptoms
4. Fever
5. Sore throat severity
6. Dysphagia
7. Odynophagia
8. Toxic appearance
9. Exam findings
10. Diagnostic testing
11. Treatment

Answer

A

VIRAL PHARYNGITIS
1. Risk factors - any
2. Onset (rapid vs. slow) - slow
3. Associated symptoms - rhinorrhea, congestion, hoarseness, ulcers
4. Fever - none or low-grade
5. Sore throat severity - mild to moderate
6. Dysphagia - possible
7. Odynophagia - none
8. Toxic appearance - No
9. Exam findings - Pharyngeal erythema, no exudate, ± tonsil hypertrophy
10. Diagnostic testing - None
11. Treatment - Supportive

INFECTIOUS MONONUCLEOSIS
1. Risk factors - Older children
2. Onset (rapid vs. slow) - Variable
3. Associated symptoms - General malaise, headache
4. Fever - High
5. Sore throat severity- MOderate to severe
6. Dysphagia - Yes
7. Odynophagia - Yes
8. Toxic appearance - Sometimes airway obstruction
9. Exam findings - Palatal petechiae, tonsil hypertrophy ± exudate, large tender cervical lymphadenopathy, splenomegaly, hepatomegaly
10. Diagnostic testing - Heterophile or EBV titres
11. Treatment - Supportive, Ibuprofen, Steroids, Rare airway obstruction

GROUP A STREPTOCOCCAL PHARYNGITIS
1. Risk factors - Peak 5-6 years old
2. Onset (rapid vs. slow) - Rapid
3. Associated symptoms - Headache, otalgia, nausea, abdominal pain
4. Fever - High
5. Sore throat severity - Severe
6. Dysphagia - Yes
7. Odynophagia - Yes
8. Toxic appearance - No
9. Exam findings - Palatal petechiae, pharyngeal erythema, tonsil hypertrophy ± exudate, large tender cervical LN, scalariform rash, strawberry tongue
10. Diagnostic testing - Rapid strep or strep culture
11. Treatment - Penicillin or Amoxicillin

DIPHTHERIA
1. Risk factors - Unimmunized
2. Onset (rapid vs. slow) - Rapid
3. Associated symptoms - None
4. Fever - High
5. Sore throat severity - Severe
6. Dysphagia -
7. Odynophagia - Yes
8. Toxic appearance - Yes, severe upper airway obstruction
9. Exam findings - Thick exudate, pharyngeal membrane
10. Diagnostic testing - Culture on tellurite media
11. Treatment - Anti toxin, PenG or Amox

Kevan Peds Question 110
Cummings chapter 201 Table 201.1

Question 43

Q

What is the typical management approach for Neisseria Gonorrhea pharyngitis?

Answer

A

Single dose Ceftriaxone / Cefixime
Always empirically treat concomitant chlamydia (single dose Azithromycin, or Doxycycline x 7 days)

Even if asymptomatic –> highly contagious

Question 44

Q

List the causative organism and clinical presentation of Herpangina?

Answer

A

Causative organisms: Coxsackievirus

Presentation: Small vesicles with erythematous bases that become ulcers and spread over the anterior tonsillar pillars, palate, and posterior pharynx, sometimes associated with cutaneous rash

Question 45

Q

List the causative organism and clinical presentation of Hand-foot-mouth disease

Answer

A

Causative organisms:
1. Coxsackievirus A16
2. Enterovirus 71

Presentation
- High fever and malaise
- Vesicular eruptions in the mouth that cause oral and throat pain
- Maculopapular rash or vesicles on the palms of the hands, soles of the feet, and buttocks

Highly contagious and should be kept away from other children

Question 46

Q

List 7 differential etiologies of pseudomembranous tonsillitis

Answer

A

Epstein Barr Virus (mononucleosis)
Group A beta-hemolytic Streptococcus
Corynebacterium DIphtheriae
Neisseria Gonorrhaea
Syphillis
Vincent’s angina: Acute necrotizing/ulcerating gingivitis/oral infection - gram-negative Fusiformis (“trench mouth”)
Candidiasis (Albicans)

Question 47

Q

What is the pathophysiology of RSV pharyngitis?

Answer

A

Viral presence in nasal cavity –> inflammatory reaction (NOT invasion) of nasal epithelium –> mucosal edema/hyperemia –> extends down into pharynx

Usually self-limited

Question 48

Q

What are the top 3 congenital laryngeal anomalies?

Answer

A

Laryngomalacia
Vocal fold paralysis
Subglottic stenosis

Question 49

Q

List a complete differential diagnosis for congenital upper airway obstruction/infantile stridor

Answer

A

A. ABOVE THE LEVEL OF THE LARYNX
1. Piriform aperture stenosis
2. Nasolacrimal duct cyst
3. Choanal atresia
4. Nasal glioma encephalocele
5. Midface hypoplasia
6. Retrognathia, micrognathia, glossoptosis
7. Macroglossia

B. LEVEL OF THE LARYNX
1. Laryngomalacia
2. Laryngeal agenesis
3. Laryngeal web
4. Vocal cord paralysis
5. Posterior glottic stenosis
6. Laryngeal cleft
7. Papillomatosis
8. Laryngeal cysts
9. Subglottic hemangioma
10. Subglottic cyst
11. Subglottic stenosis

C. BELOW THE LEVEL OF THE LARYNX
1. Vascular ring/extrinsic tracheal compression
2. Tracheal stenosis
3. Complete tracheal rings
4. Tracheomalacia
5. Laryngotracheoesophageal clefts
6. TEF

Question 50

Q

What is the most common cause of infant stridor?

Answer

A

Laryngomalacia

Question 51

Q

What is the most common laryngeal anomaly/disorder?

Answer

A

Laryngomalacia

Question 52

Q

Regarding laryngomalacia, discuss:
1. Cause
2. Risk Factors
3. Factors influencing development of laryngomalacia
4. Clinical Presentations
5. Complications/severe signs
6. Diagnostic workup

Answer

A

CAUSES:
- Hypotonia of immaturity causes collapse of bulky infantile tissues, causing airway obstruction

RISK FACTORS:
1. Prematurity
2. Hypotonia
3. Neuromuscular disorders
4. GERD (possible aggravator vs sequelae?)
5. Hispanic/Black ethnicity

FACTORS INFLUENCING DEVELOPMENT OF LARYNGOMALACIA:
1. Shortened aryepiglottic folds (15%)
2. Anterior collapse of cuneiform cartilage (60%)
3. Posterior epiglottic collapse (10%)
4. Immature neuromuscular control
5. Reflux (60%)

CLINICAL PRESENTATION:
1. Onset 2 weeks to 1 year old
2. Usually self-resolves by 1 year as child grows (median resolution 7-9 months; major 18mos resolved)
3. Inspiratory stridor (may be the only symptom in mild)
4. Worsens with feeding, supine position, with H/N flexed
5. Better with prone, H&N extended, crying (increases pharyngeal tone) - except if severe, then collapse worse with crying
6. Commonly also have GERD symptoms (choking/arching with feeds, reflux) which aggravates airway edema
- Respiration against obstruction increases negative intrathoracic pressure, this increases reflux, which increases swelling, which increases obstruction (perpetuating cycle)

COMPLICATIONS/SEVERE SIGNS (< 5%)
1. Feeding difficulties
2. Apneas/cyanosis
3. Pectus excavatum
4. Cor pulmonale
5. Pulmonary HTN
6. Failure to thrive

DIAGNOSTIC WORKUP - FNL findings:
1. Long, tubular, omega-shaped epiglottis
2. Short AE folds
3. Large, floppy arytenoids
4. 15% synchronous lesion (tracheomalacia and SGS most common) contributing to symptoms
- Bronchomalacia, pharyngomalacia, vallecular cyst less common

Question 53

Q

Describe the classification system for laryngomalacia

Answer

A

OLNEY CLASSIFICATION (1999):
1. Type 1: Anterior collapse of cuneiform cartilage
2. Type 2: Shortened aryepiglottic folds
3. Type 3: Redundant arytenoid tissue
4. Type 4: Omega epiglottis

MECHANISM-BASED:
1. Anterior = epiglottis
2. Posterior = large arytenoids
3. Lateral = AE folds

ANATOMIC (Holinger/Konier) CLASSIFICATION (1989):
I: Inward collapse of AE folds / cuneiform
II: Long, tubular epiglottis folds on itself
III: Anterior, medial collapse of arytenoid cartilages
IV: Posterior displacement/collapse of epiglottis
V: Short AE folds

Question 54

Q

Discuss the management options for laryngomalacia.
What are the indications and contrainidications for surgical intervention such as supraglottoplasty?
What are the complications of a supraglottoplasty?
What are the indications for tracheostomy in Laryngomalacia?

Answer

A

A. OBSERVATION (if no worrisome signs/complications)

B. CONSERVATIVE
1. Prone positioning
2. Upright feeding
3. Consider NG feeds
4. Thickened feeds
5. Small, frequent feeds

C. MEDICAL
1. PPI - 1mg/kg/day (increase to BID if severe) ± H2 receptor antagonist
2. CPAP

D. SURGICAL (Improves stridor but does not disappear - gets out of “danger zone” to allow them to grow out
1. Rigid bronchoscopy FIRST to rule out any secondary airway lesions
2. Supraglottoplasty options (using cold steel, laser CO2/KTP, or electrocautery)
- Trim epiglottis partially
- Divide AE folds (usually first)
- Trim redundant mucosa from post-surface of arytenoid cartilages (prevent posterior glottic stenosis)
- Removal of cuneiform & corniculate cartilages
3. Epiglottopexy (secure to BOT - “glossoepiglottic adhesion)
4. Tracheostomy

Absolute Indications for Surgery:
1. Failure to improve on conservative/medical management
2. Any of the severe signs/complications
- Cor pulmonale
- pHTN
- Hypoxia
- Apnea
- Recurrent cyanosis
- FTT
- Pectus excavatum
- Stridor with respiratory compromise
- Stridor with significant retractions

Relative Indications for Surgery:
1. Aspiration
2. Difficult to feed, failing medical therapy
3. Weight loss with feeding difficulty

Contraindications for Surgery:
1. Several comorbidities
2. Multi-level airway obstruction
3. Postpone if URTI (reactive airways)
4. Weight and age generally are NOT contraindications

Indications for tracheostomy:
1. > 3 comorbidities
2. Severe sleep apnea
3. Worsening symptoms post-revision supraglottoplasty

Complications of supraglottoplasty:
1. Bleeding, infection, anesthesia
2. Temporary worsening of airway symptoms secondary to edema
3. Temporary dysphagia
4. Granulation tissue
5. Glottic web formation
6. Aspiration
7. Trauma to surrounding structures
8. Subglottic stenosis
9. Supraglottic stenosis (< 5% if bilateral; preserve islands of mucosa in interarytenoid area)
10. Posterior glottic stenosis
11. Insufficient release (need for further surgery) - 15% if unilateral
12. Worsening obstruction from excessive tissue removal causing massive collapse - “less is more”

Question 55

Q

How does Laryngopharyngeal reflux different from classic GERD?

Answer

A

Patients have head and neck symptoms, but heartburn is uncommon
Predominantly upright (daytime) reflux
Normal esophageal motility
Most do not have esophagitis, as in GERD
Laryngopharyngeal epithelium is more susceptible to reflux related injury than esophageal epithelium

Question 56

Q

What are the six evaluations for laryngopharyngeal reflux (LPR) in pediatrics?

Answer

A

24-hour double-probe pH monitoring (Gold Standard)
Gastric emptying scan (milk scan) technetium 99m
Esophageal manometry
Barium swallow
Broncho-alveolar lavage for lipid laden macrophages (70% needed)
Esophagogastroduodenoscopy with Biopsy (EGD, suspected eosinophilic esophagitis)
Diagnostic markers: pepsin & carbonic
anhydrase isoenzyme III (CA-III) –> acquired from laryngeal biopsy (not yet clinically used)

Question 57

Q

What are the most common reflux related laryngeal disorders in pediatrics?

Answer

A

Chronic cough
Hoarseness
Aspiration
Recurrent croup
Laryngomalacia
Episodic laryngospasm
Subglottic stenosis

“CHARLES”

Question 58

Q

What is laryngeal dyskinesia in kids?

Answer

A

Presents with mild stridor
Associated with GERD
Resolve by 1 year of age
Distinct from adductor paralysis

Question 59

Q

What is the suspected underlying causes of SIDS? What is the recommended positioning for infants?

Answer

A

SIDS = Sudden infant death syndrome

Suspected Cause:
- Laryngeal chemoreflex/adductor reflex = laryngospasm in response to laryngeal reflux
- Protective in adults (aspiration prevention)
- In infants, can cause prolonged apnea, bradycardia, and CV arrest
- Worse in hypoxic states (more severe reflex)

Laryngeal chemoreflex triggered by:
- Carbohydrates
- Milk
- Acid stimulation of pharynx
- CO2 level
- Airflow/pressure or humidity/temperature changes

Recommended positionining:
1. Supine/side positioning preferable to prone (decreases hypercarbia associated with prone position)

Question 60

Q

What are options for ventilation during supraglottoplasty?
What are some additional anesthetic considerations for this procedure?

Answer

A

Spontaneous ventilation (most common)
Supplemental blow-by oxygen via NG
O2 via bronchoscopy
Jet ventilation
Intermittent BMV
Intermittent intubation
Small ET tube

Other anesthetic considerations:
1. Spray topical lidocaine on cords (avoid laryngospasm)
2. 0.5mg/kg decadron
3. Intubate if unstable or patients with poor pulmonary reserve

Question 61

Q

List a differential diagnosis for causes of infant vocal fold paralysis

Answer

A

A. CONGENITAL
1. Arnold Chiari malformation (lower part of brain pushes down into spinal canal)
2. CNS abnormality (central or peripheral)

B. INFECTIOUS
- Syphillis

C. IDIOPATHIC (47%, especially bilateral)

D. IATROGENIC
- CVS surgery
- PDA ligation
- Tracheoesophageal fistula repair
- Chemotherapy: Vincristine (interferes with microtubular assembly, rare, majority bilateral)

E. TRAUMA
- Surgery (cardiac, TEF, thyroid, neck): e.g. branchial anomalies, PDA ligation 1-7.4%, aortic arch repair
- Birth trauma (traction type neck injury associated hematoma/soft tissue swelling/compression to vagus) - recovery > 9 months
- Trauma from intubation or aggressive suctioning

F. NEOPLASTIC
1. Brain/brainstem tumor
2. Vascular anomaly

G. NEUROLOGIC (Central or peripheral)
1. Moebius - affects muscles of facial expression and eye movement
2. Charcot Marie Tooth - Hereditary motor & sensory neuropathy (>50% bilateral)
3. Hydrocephalus
4. Cerebral palsy
5. Meningomyelocele
6. Hypoxic encephalopathy
7. Hypotonia

THREE MOST COMMON:
1. Idiopathic
2. Arnold Chiari malformation
3. Birth trauma

Question 62

Q

What are the most common causes of bilateral infantile vocal fold paralysis?

Answer

A

Idiopathic
Birth trauma
Arnold Chiari
Increased ICP (e.g. hydrocephalus)
Neuropathy of prematurity

Question 63

Q

After how long of vocal fold paralysis in children will return of function be unlikely?

Question 64

Q

Regarding infantile vocal fold paralysis, discuss:
1. What is the clinical presentation?
2. What is the work-up?

Answer

A

Clinical presentation:
1. Weak cry
2. Stridor
3. Aspiration
4. Dysphagia
5. Feeding difficulties

Work-up:
1. Bedside FNL to confirm diagnosis while awake (time with breathing to rule out paradoxical VF motion)
2. MRI entire path of RLN (r/o brain/nerve abnormality)
3. Genetics: idiopathic congenital bilateral VFP
4. Direct laryngoscopy - palpate CA joint (rule out fixation)
5. Pediatric laryngeal electromyography

Answer 63

A

Problem is aspiration in unilateral VFP - therefore need to address this

TREATMENT OPTIONS:
A. Observation if not struggling (most will spontaneously recover)
B. Conservative:
1. OT/PT/SLP - r/o aspiration
2. Slow-flow nipple
3. Thickened feeds
4. NG
5. G-tube

C. Surgical
- VC injection medialization (short term injectables preferred during infancy, such as carboxymethylcellulose)
- Type 1 thyroplasty (ONLY for older children who show no recover - vocal cords are lower than adults, child may not be able to cooperative with intraop tuning)
- Re-innervation procedures

PROGNOSIS
- 70% idiopathic self-resolve by 6 months
- 35% surgical

Answer 64

A

Problem is airway in bilateral VFP

CONSERVATIVE
1. OT/PT/SLP - rule out aspiration
2. Slow flow nipple
3. Thickened feeds
4. NG
5. G Tube

CONSERVATIVE/MEDICAL
1. CPAP / positive pressure ventilation
2. ETT

SURGICAL
1. Vocal cord lateralization (Type II Isshiki)
2. Posterior costal cartilage graft (to separate arytenoids)
3. Laser cordotomy (transverse cut between vocal process and vocal fold)
4. Tracheostomy
5. Nerve reanimation techniques/external larygngeal pacing (Neuromuscular pedicle transposition to PCA)

Procedures to be done at least after 1 years old:
- Partial cordotomy
- Unilateral cordectomy
- Arytenoidopexy: Plicating vocal process to external laryngeal framework (woodman lateral approach, or anterior thyrotomy approach)
- Arytenoidectomy: Endolaryngeal (UL/BL, laser partial, or total), Extralaryngeal (woodman lateral approach, or anterior thyrotomy approach)

PROGNOSIS
1. 65% Idiopathic self-resolve by 36 months (better if no associated anomalies)
2. Persistence > 2-3 years - often incomplete laryngeal muscle atrophy, CA fixation, synkinesis

Vancouver 472

Answer 65

A

Type I: Protrusion of cerebellar tonsils (can be asymptomatic until adolescence/adulthood)
- Presents in 25-35 year old
- > 5mm hernation
- Headache, neck pain, facial pain, extremity weakness, sensory complaints, unsteadiness
- Can have uni/bilat HL, tinnitus, vertigo, disequilibrium
- Down-beating nystagmus
Type II: Protrusion of cerebellar vermis, lower pons, and medulla (Arnold-Chiari malformation) - spina bifida
- Presents in first few months of life with VF paralysis
Type III: Herniation of cerebellum (high cervical meningocele) - Rare
Type IV: Cerebellar Hypoplasia (Dandy-Walker Syndrome) - Rare

Answer 66

A

CN IX-XII difficulties
Bilateral vocal fold paralysis, Respiratory distress
Poor feeding
Aspiration

Answer 67

A

Risk factors:
- Female
- Teenager
- Competitve athletes
- Anxiety/stress
- Triggered during high intensity, resolves when stops
- Also seen in benign rolandic epilepsy

Pathophysiology: ?Laryngeal hyperresponsiveness associated with GERD

Answer 68

A

Laryngeal webs are on the sepctrum of laryngeal atresia

Types:
1. Glottic (anterior & posterior): 75%
2. Subglottic < 10%
3. Supraglottic < 5%

Answer 69

A

Flexible laryngoscopy
± Rigid laryngoscopy + bronchoscopy (site, thickness, horizontal and vertical extent)
± X-ray (Sail sign = persistent tissue between Vocal cords and subglottis, rule out SGS)
± FISH for anterior glottic web (22q11.2 deletion)

Answer 70

A

ASSOCIATIONS:
1. 22q11 deletion (VCF, DiGeorge) - 65%
- Look for CATCH-22 features (e.g. cardiac defects, abnormal facial features, thymic hypoplasia, cleft palate, hypocalcemia)
- Conotruncal heart malformations
2. Pallister Hall - CLI3 gene chromosome 7
- Midline problems: Hypothalamic anomalies, anterior glottic webs, posterior laryngeal clefts, bifid epiglottis, imperforate anus
3. Richieri-Costa Pereira Syndrome
- Microwebs
- Epiglottis absence/hypoplasia
- Small round larynges
- Arytenoid/AE hypertrophy

CLINICAL PRESENTATION:
1. Stridor
2. Aphonia
3. Severe webs - often have a thick cartilaginous component involving cricoid cartilage inferiorly “subglottic sail configuration”

COHEN’S CLASSIFICATION OF CONGENITAL GLOTTIC WEBS/STENOSIS
1. Type 1: < 35% obstruction with none or little subglottic involvement
2. Type 2: 35-50% obstruction with little subglottic extension
3. Type 3: 50-75% obstruction, thin-thick web with some extension to lower border of cricoid (usually thick anteriorly, and thins out posterior)
4. Type 4: 75-90% obstruction, thick web extends to lower cricoid

TREATMENT:
1. Tracheostomy if needed to protect airway
2. Endoscopic procedure: endoscopic typically reserved for early-stage Cohen Type I-II webs:
- Web division ± serial dilatations
- Web division ± stenting
- Web division ± Mitomycin C injection
3. Open procedure: for more advanced stage lesions (Type III-IV) typically to also address subglottic extension
- Laryngofissure + stent/mold/keel
- Laryngotracheoresection ± cartilage grafting (single stage vs. double stage)

Answer 71

A

DIAGNOSIS:
1. May involve cricoarytenoid joint and mimic vocal fold paralysis, therefore need to differentiate from VFP by palpation of interarytenoid space

BOGDASARIAN CLASSIFICATION:
I: Interarytenoid scar band with normal posterior commissure (gap seen behind the scar band)
II: Interarytenoid scar band involving the posterior commissure with no posterior gap seen
III: Posterior commissure stenosis + unilateral cricoarytenoid fixation
IV: Posterior commissure stenosis + bilateral cricoarytenoid fixation

TREATMENT:
1. Tracheostomy
2. Web division (often recurs/scars)
3. Arytenoidectomy
4. Laryngotracheal resection

Kevan Pediatrics Question 146

Answer 72

A

Complete absence of laryngeal lumen
- I: Supraglottic + infraglottic
- II: Infraglottic
- III: Glottic

Answer 73

A

GENETICS:
1. Deletion chromosome 5p

EPIDEMIOLOGY:
1. 1/50000 births

FEATURES:
A. CNS
1. Microcephaly
2. Hypotonia
3. Developmental delay

B. ENT
1. High pitched stridor (cat like cry)
2. Hypertelorism
3. Broad nasal root
4. Micrognathia

Laryngoscopy findings:
1. Elongated epiglottis
2. Narrowed diamond-shaped glottis
3. Interarytenoid muscle paralysis

Vancouver 476

Answer 74

A

VALLECULAR CYST = Lesion occupying vallecula, originating either from lingual surface of the epiglottis or base of tongue. Two main types:
1. True Vallecular cyst: Arising from supraglottic larynx on surface of the epiglottis
2. Lingual TGDC: Arises from foramen cecum at base of tongue (tubule remnant that fails to obliterate after thyroid descent)
- Not translucent
- Occur higher in vallecula than true laryngeal vallecular cyst
- Histology: Pseudostratified ciliated or squamosu epithelium of thyroglossal duct origin; mucous glands & thyroid follicles may be present in subjacent stroma

CLINICAL PRESENTATION (depends on size)
- Stridor
- Feeding difficulty/coughing
- Cyanotic episodes
- FTT
- Breath-holding spells
- Normal or muffled voice
- Lingual TGDC symptoms occur during first few weeks of life
- Inflammation/infection cause rapid expansion –> airway obstruction

DIAGNOSIS:
1. Flexible/direct laryngoscopy
2. CT/MRI
- Vallecular cyst: T1 hypointense, T2 hyperintense
- Lingual TGDC: T1 hyperintense, T2 iso or hyperintense

DIFFERENTIAL:
1. Dermoid
2. Teratoma
3. Lingual thyroid (u/s to confirm normal thyroid)
4. Lymphatic malformation
5. Hemangioma

TREATMENT:
1. Endoscopic removal
2. Marsupialization
3. Do not aspirate - increases likelihood of recurrence (unless emergency surgical circumstances)

Answer 75

A

CAUSE:
- Failed fusion of posterior cricoid lamina or interarytenoid tissue at 6 weeks GA
- Leads to incomplete development of tracheo-esophageal septum

BENJAMIN-INGLIS CLASSIFICATION (most common):
1. Type 1: Interarytenoid
2. Type 2: Into cricoid cartilage (but does not go through cervical trachea)
3. Type 3: Through cricoid cartilage into cervical trachea, but not thoracic trachea
4. Type 4: Into thoracic trachea
5. Other: Occult/submucous - often associated with subglottic stenosis, easily missed, detected on palpation, posterior midline cartilage defect

EVAN’S FUNCTIONAL CLASSIFICATION
Same as Benjamin Iglis classification, except Type 2 is the BI Type 2+3, and Type 3 is BI Type 4

MEYER-COTTON CLASSIFICATION:
L = Laryngeal; LT = Laryngotracheoesophageal
1. L1 = Interarytenoid
2. L2 = Into cricoid cartilage
3. L3 = Through entire cricoid cartilage, not involving trachea
4. LT1 = Into cervical trachea
5. LT2 = Into thoracic trachea

CLINICAL PRESENTATION
1. Aspiration
2. Chronic cough
3. Feeding difficulties
4. Recurrent pneumonia
5. Stridor
6. Respiratory distress

SYNDROMES:
1. Pallister Hall Syndrome
2. Opitz-Frias Syndrome
3. TEF (25%)
4. VATER/VACTERL
5. CHARGE
6. Velocardiofacial syndrome
7. Bamforth Lazons

ASSOCIATED ANOMALIES:
1. Esophageal atresia ± TEF (most common) - 6% of TEFs have clefts, continued aspiration
2. Cleft lip/palate
3. CHD, GI anomalies
4. Opitz G Syndrome - Hypertelorism, Hypospadias, Cleft lip/palate
5. Pallister Hall Syndrome - Bifid epiglottis, hypothalamic hamartoblastoma, hypopituitarism, imperforate anus, postaxial polydactyly

DIAGNOSIS:
1. Laryngoscopy with palpation
2. BAL to look for lipid-laden macrophages (for signs of aspiration)
3. Barium swallow
4. CXR (chronic aspiration/pneumonia)
5. Flexible fiberoptic laryngoscopy & FEES

TREATMENT
1. Conservative
- PT/OT/SLP: Behavioural modifications
- Thickened feeds
- PPI

Surgical
- Type 1-2: Injection laryngoplasty or endoscopic repair with 2-layer closure
- Type 3-4: Anterior laryngofissure ± interposition flap

MANAGEMENT BY GRADE:
1. Type I: Observation, anti-reflux & thickened feeds; vs. endoscopic repair (CO2 laser with suture or filler augmentation described)
2. Type II or III: Laryngofissure for precise multilayered anatomic closure, consider endoscopic approaches
3. Type IV: Laryngofissure & Sternotomy vs. lateral pharyngotomy & Thoracotomy (Requires ECMO without an ETT)

Vancouver 477

Answer 76

A

INHERITANCE: X-linked
Gene: MID1 chromosome Xp22
Protein: Midline-1

FEATURES:
1. Hypertelorism
2. Cleft lip/palate
3. Bifid uvula
4. Micrognathia
5. Laryngeal cleft
6. Hypospadias

Answer 77

A

Inheritance: Autosomal Dominant
Gene: GL13 chromosome 7p14

FEATURES “PHIL”:
1. Polydactyly
2. Hypothalamic abnormalities, hypopituitary
3. Imperforate anus/anal atresia
4. Laryngeal clefts and bifid epiglottis

Vancouver 477

Answer 78

A

INHERITANCE: Autosomal recessive
GENE: FOXE1, Chromosome 9q22
PROTEIN: Thyroid transcription factor 2 (TTF-2)

FEATURES:
1. Spikey hair
2. Cleft palate
3. Bifid epiglottis
4. Choanal atresia
5. Thyroid agenesis

Vancouver 478

Answer 79

A

Thyroid function tests (Bamforth syndrome)
Pituitary work up (Pallister hall syndrome)

Answer 80

A

Quadrivalent: 6, 11, 16, 18

Gardasil 9: 6, 11, 16, 18, 31, 33, 45, 52, 58

Answer 81

A

All girls and boys ages 11-12 (Grade 6)
Catch up vaccine
- Girls 13-26 years of age
- Boys 13-21 years of age

Answer 82

A

CAUSE: HPV 6 and 11 (more aggressive)
- Also 16 and 18
- Human Papilloma Virus = Double stranded DNA virus

PATHOPHYSIOLOGY:
- Virus infects stem cells of basal cell layer –> integrates into host DNA –> activates EGF –> induces rapid epithelial proliferation –> injury to surrounding normal epithelium may cause implantation and spread

HISTOLOGY:
- Microscopic histology:
a. Finger-like papillary fronds (projections)
b. Fibrovascular core
c. Non-keratinizing squamous epithelium
d. Superficial spreading pattern (“velvety”)
- Koilocytosis (vacuolation of HPV-infected epithelial cells) - superfiical cells with dense, small or atypical nuclei and perinuclear halo - indicative of viral infection
- Macroscopic: Exophytic (“cauliflower”)

NATURAL HISTORY:
1. Spontaneous regression
2. Not associated with puberty

Chapter 208 Fig 208.1

Answer 83

A

RRP is the second most common cause of hoarseness in children

JUVENILE ONSET RRP (Defined as < 12 years; Usually < 5 years old)
- Vertically acquired from birth tract (risk 1:80 to 1:500)
- More common, more aggressive
- Often subsides by puberty

Risk Factors:
1. First born (due to prolonged second stage of labor) - 75% of cases first born
2. Young mom (teenage)
3. Vaginal delivery
4. Recent genital HPV infection
5. Presence of genital warts (1:400)
6. Prolonged labour (2nd stage)
7. HPV Type 11
8. Tracheostomy
9. Immunocompromised

ADULT ONSET RRP (Defined as >12 years old onset; Usually 20-40 years old)
- Sexually acquired
- Less common, more indolent course
- Chronic, doesn’t resolve

Risk Factors:
1. Oral sex
2. Multiple sexual partners (> 26)

CLINICAL PRESENTATION:
1. Progressive hoarseness (most common)
2. Stridor
3. Respiratory distress

PREFERENTIAL SITES:
Squamo-columnar junctions most common - transition points from squamous to respiratory epithelium
1. 15-30% shows distal/multisite spread
2. Laryngeal & midline surface of epiglottis
3. Laryngeal ventricle (esp. upper and lower ventricle margins)
4. Undersurface of vocal cords
5. Carina
6. Tracheostomy stoma (iatrogenic implantation - creates a junction between squamous and respiratory epithelium)
7. Nasopharyngeal surface of soft palate
8. Bronchial spurs
9. Nasal vestibule = stratified squamous
- Transitional point (limen vestibuli marks the transition point)

Answer 84

A

30% children
15% adult

Answer 85

A

SURGICAL: Repeated debulking (standard of care)
1. Cold steel for singular/focal lesions
2. Laser: CO2, Thulium laser (2013nm, cutting/ablating), Photoangiolytic lasers (Pulsed-dye, KTP, argon, Nd-Yag)
3. Microdebrider - superior voice outcome
4. Phono-microsurgery (rarely used)
5. Biopsy periodically to subtype virus and rule out risk of malignancy

AIRWAY MANAGEMENT:
1. AVOID tracheostomy if at all possible - Risk seeding distal airways (95%, vs 15% without tracheostomy)
- Newer literature suggests: need for tracheostomy may be a marker of more severe disease rather than an independent cause of distal spread

ADJUVANT TREATMENT (10% will require some form)

Indications:
1. More than 4 surgeries/year
2. Aggressive disease or risk of airway obstruction
3. Distal/multisite spread

Options for adjuvant treatment
1. Bevacizumab (Avastin) - VEGF inhibitor
2. Intralesional Cidofovir - antiviral, disrupts DNA replication; side effect = nephrotoxic
3. Other antivirals: Acyclovir, Ribavirin
4. Interferon-alpha (risks/side effects: fever, headache, nausea, myalgias, febrile seizure, leukopenia, growth retardation, hepatotoxicity, CP if given < 1yo) - cytokine, antiviral
5. Indol-3-carbenol (found in cabbage) - negative regulator of estrogen (estrogen increases HPV gene expression and allows for epithelial proliferation) - possibly less effective now in studies
6. Photodynamic therapy - transfer of energy to a photosensitive drug such as dihematoporphyrin ether which has a tendency to concentrate within papillomas
7. Anti-reflux therapy
8. Therapeutic vaccination
9. Celebrex (COX-2 inhibitor, inhibits arachidonic acid to prostaglandin precursors, which HPV interacts with) - so far less effective
10. Gefitinib (Anti-EGFR Tyrosine kinase inhibitor - investigational

INVESTIGATIONAL:
1. PD-1 inhibitors (Pembrolizumab)
2. HPV vaccine
3. Mumps vaccine
4. Retinoic acid (so far less effective)

PREVENTION
1. Routine C-section NOT recommended (even with active infection risk of RRP 1/400 - this is lower than the risks associated with C-section) - Vancouver notes say can consider in young, primiparous mothers with recent HPV infection and genital warts
2. HPV vaccine

Answer 86

A

No aerosolization of HPV virus
Quicker set up
No thermal injury
Lower cost
No risk of airway fire
Better voice outcomes (controversial)

Answer 87

A

HPV Type 16, 18
Smoking
Radiotherapy in childhood

Answer 88

A

A. CONGENITAL
1. Ellipital cricoid
2. Down Syndrome

B. IDIOPATHIC

C. INFECTIOUS
1. Bacterial
2. Fungal

D. INFLAMMATORY
1. GERD

E. TRAUMATIC
1. Prolonged intubation
2. Surgical injury
3. High tracheostomy
4. Cricothyrotomy
5. Burns

F. TOXINS
1. Caustic ingestion

G. NEOPLASTIC
1. Hemangioma
2. Benign vs. malignant
3. Intrinsic vs. extrinsic

H. SYSTEMIC
1. Wegener’s
2. Sarcoid
3. Relapsing Polychondritis

Answer 89

A

4.5-5mm in diameter
3-4mm in premature
Size 3 ETT

SGS at term = < 4mm
Premature = < 3mm

Answer 90

A

Q = Flow rate
P = Pressure
r = radius
n = fluid viscosity
l = length of tubing

Q = (pi x P x r^4) / (8 x n x l)

Answer 91

A

Based on endoscopic appearance:
1. Anterior
2. Posterior
3. Lateral shelves
4. Circumferential
5. Complete

Answer 92

A

Soft tissue (granulation tissue, submucosal gland hyperplasia, submucosal fibrosis)
Cartilaginous, normal shape (Cricoid small for infant’s size)
Cartilaginous, abnormal shape (Elliptical, large anterior lamina, large posterior lamina, generalized thickening, submucous/incomplete laryngeal cleft, other)
Cartilaginous (trapped first tracheal ring)
Combined stenosis

Answer 93

A

Congenital = no history of ETT or laryngeal trauma
Congenital caused by failure or incomplete recanalization of the laryngeal lumen at 10 weeks gestation

Acquired has worse symptoms and prognosis; congenital tends to improve with growth of the child

Answer 94

A

COTTON MEYER GRADING
1. Grade 1: 0-50%
2. Grade 2: 51-70%
3. Grade 3: 71-99%
4. Grade 4: Complete obstruction

Neonates: failure to pass 4mm telescope = SGS

Answer 95

A

PRESENTATION:
1. Recurrent croup
2. Frequent / prolonged URTIs
3. Airway: biphasic stridor, air hunger, increased work of breathing
4. Feeding: poor feeding, dysplagia, aspiration
5. Voice: Strange cry, hoarse, aphonic

WORKUP:
1. Term neonate: Failure to pass a 4mm telescope
2. Serial ETT: Start small and work up until no further air leak (largest one with a leak is the correct size)

Answer 96

A

A. OBSERVATION
- If Grade I-II with minimal symptoms, reliable follow up (especially congenital)
- Repeat bronchoscopy q 3-6 months

B. MEDICAL OPTIONS
1. Steroids
- May reduce acute inflammation
- May reduce scarring, prevent worsening stenosis
- May increase infection risk, increasing recurrence
- May cause cartilage resorption, worsening stenosis
2. Epi nebs
- For acute exacerbations
3. Heliox
- Temporizing measures
4. PPI
- Decrease aggravating factors

C. SURGICAL OPTIONS
1. Tracheostomy

Balloon dilations
- Only good for early soft tissue stenosis
- ± Mitomycin C injection
- ± Steroid injection
Endoscopic CO2 laser OR cold steel
- CO2 only good for small, isolated scar bands
Anterior cricoid split + cartilage graft
- Only for intubated neonates to facilitate extubation (not frequently done anymore, was more common when they used different more inflammatory ETTs)
- Now when done usually accompanied by grafting
- Goal is to relieve pressure and increase venous bloodflow
- Minimal actual airway widening: 1-2mm
- Options: (1) Split and leave cartilage open, cover with soft tissue, or (2) Cartilage interposition graft (3mm distraction)
Posterior Cricoid split ± cartilage graft
Four Quadrant technique
LTR/LTP (see other card)
Slide tracheoplasty (see other card)
Cricotracheal resection (see other card)

Answer 97

A

“Factors that predispose to failure in treating subglottic stenosis with a CO2 laser”

When there is risk of inducing worse scarring with the procedure, such as:

Circumferential cicatricial scarring
Abundant scar tissue >1cm in the vertical dimension
Fibrotic scar tissue in the interarytenoid area of the posterior commissure
Cartilaginous stenosis
Loss of cartilaginous framework
Infection of trachea after tracheotomy
Exposure of perichondrium or cartilage during CO2 laser excision, predisposing to perichondritis and chondritis
Combined laryngo-tracheal stenosis
Concomitant tracheal disease
Previous endoscopic management failure

Answer 98

A

Laryngeal mask airway
Heliox
Spontaneous breathing (induction via inhalational mask, then TIVA anesthetic)
Intermittent extubation
Jet ventilation (adults only)

Answer 99

A

INDICATIONS:
1. Failure of extubation 2 times in neonate/young child
2. Congenital small cricoid in older child

CONTRAINDICATIONS:
1. Short duration of extubation before reintubation (hours)
2. Peak airway pressure > 35mmHg

Answer 100

A

Indication: Restricted to neonates or young infants whose pathology is limited to swelling of the glottis and/or subglottis that causes multiple failed extubation attempts

Candidate for Anterior cricoid split if:
1. Minimum weight 1500g
2. At least 2 failed extubation attempts
3. No ventilator support for several days (at least 10)
4. Minimal (< 30%) FiO2 supplement
5. No CHF to would preclude use of steroids (for 30 days)
6. No Antihypertensive medication use that could preclude use of steroids (for 10 days)
7. No acute respiratory infection (that would prolonged intubation after cricoid split)

Most criteria essentially get at the fact that they basically need to be extubatable in all other respects, and its just the subglottic stenosis limiting them.

chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.optecoto.com/article/S1043-1810(09)00075-X/pdf

Answer 101

A

3mm
- Generally, cartilage grafts are taken from thyroid ala, rib, or conchal cartilage
- Most procedures these days receive a graft

Answer 102

A

CAUSES:
1. Primary: Complete tracheal rings, Down’s syndrome, Pfeiffer syndrome
2. Secondary: similar to SGS

MCCAFFREY GRADING OF LARYNGOTRACHEAL STENOSIS (most common):
1. Grade 1: Confined to subglottis, < 1cm length - treat with dilation alone
2. Grade 2: Confined to subglottis, > 1cm length
3. Grade 3: Subglottic stenosis (>1cm) extending into the trachea, not involving glottis
4. Grade 4: Similar to stage 3, but also extension into glottis with unilateral or bilateral cord fixation

CANTRELL & GUILD CLASSIFICATION OF CONGENITAL TRACHEAL STENOSIS:
1. Type 1: Generalized hypoplasia of entire trachea
2. Type 2: Funnel stenosis (normal proximal trachea + distal narrowing)
3. Type 3: Segmental, up to 3 rings involved

CLINICAL PRESENTATION:
- Biphasic stridor
- Atypical asthma
- Recurrent croup/pneumonia

DIAGNOSIS:
1. Bronchoscopy: assess diameter, length, degree, character (beware inducing airway obstruction from intraoperative trauma/manipulation!)
2. CT or MRI

TREATMENT OPTIONS (Surgical):
1. Endoscopic: Balloon or serial dilations, cold knife, laser, stents
2. Laryngotracheoplasty or Laryngotracheal reconstruction (LTP/LTR)
3. Cricotracheal resection
4. Slide tracheoplasty

https://www.researchgate.net/publication/338454610/figure/fig2/AS:11431281154097876@1682677360041/McCaffrey-Classification-The-stenosis-can-be-located-in-the-subglottis-or-in-the-trachea.tif

Answer 103

A

Indications:
1. > 10kg
2. Grade 1-4 stenosis

SINGLE STAGE PROCEDURE:
- Description: Decannulate at time of procedure, use ETT for 7-14 days as stent, monitor in PICU

A. Indications:
1. Older child
2. Stomal/tracheostomy problems

B. Advantages:
1. No tracheostomy (decannulate in OR)
2. Single OR

C. Disadvantages:
1. ICU admission (5-10 days) with significant sedation, withdrawal issues post-extubation
2. Risk re-intubation and tracheostomy
3. Risk of hospital acquired pneumonia
4. Risk of self-extubation if not sedated enough (need a good experienced ICU for this to balance sedation)

DOUBLE STAGE PROCEDURE:
- Description: Leave tracheostomy in situ, place a stent, return in 6 weeks for stent removal and decannulation

A. Indications:
1. Poor lung function
2. Medical comorbidities
3. Complicated surgery
4. Severe stenosis
5. Previous failed procedures
6. Difficult reintubation
7. Poor ICU support / facilities
8. History of sedation issues

B. Advantages:
1. No ICU
2. Shorter hospital stays
3. Avoid sedation/withdrawal issues

C. Disadvantages:
1. Multiple ORs (stent & tracheostomy left in place; stent removed @ 6 weeks, tracheostomy removed @ same time 6 weeks, or possibly at 12 weeks)
2. Increase risk of tracheostomy/stent complications (e.g. granuloma, etc.)
3. Reliant on tracheostomy as only airway

APPROACHES (Single or Double stage)
A. Anterior Graft; indications:
1. Anterior SGS
2. Mild circumferential SGS
3. Stomal tracheomalacia (cap graft)

B. Posterior Graft; indications:
1. Posterior SGS
2. Isolated subglottic shelves
3. Circumferential subglottic stenosis
4. Total or near total obstruction
5. Bilateral VF paralysis (VF splaying)

C. Anterior & Posterior Grafts; indications:
1. Lateral shelves SGS
2. Circumferential SGS

MAXIMUM GRAFT WIDTH (for all approaches) = 4mm (or risk inducing aspiration if too large)

SUCCESS RATES:
1. Grade 1-2: 90%
2. Grade 3: 70%
3. Grade 4: < 40% (therefore consider CTR)

See Half day lecture on airway anomalies for images

Answer 104

A

Posterior glottic/subglottic stenosis
Complete glottic/subglottic stenosis
Significant cricoid deformity

“PCS = Posterior cricoid split”

Answer 105

A

STUNK:
1. S: Severely altered anatomy by stenosis or surgery
2. T: Tracheomalacia (lack of airway wall rigidity)
3. U: Unstable cartilage grafts
4. N: No cartilage graft with posterior cricoid split
5. K: Keloid formation

Answer 106

A

Grade III and IV
Congenital elliptical cricoid

PROCEDURE:
- Division of anterior and posterior walls (± grafts) + lateral wall of cricoid (anterior to inferior cornu of thyroid, and extraperichondrial externally to avoid RLN)
- Aboulker or Cotton-Lorenz Stent for 6 months (Very unstable airway)

Answer 107

A

Difference between this and LTR
LTR - split the cricoid and trachea and place graft to reconstruct
CTR - Complete resect the cricoid, leaving the posterior plate, and then reanastomosing the rest (sometimes need Grillo stitch to keep neck flexed to avoid dehiscence)

INDICATIONS:
1. Severe stenosis (Grade 3-4)
2. Short segment stenosis
3. > 3mm from VCs (otherwise risk creating SGS)
4. Failed LTP

RISKS:
1. RLN injury
2. Dehiscence
3. SGS (if < 3mm from VF)

SUCCESS RATE: Grade 4 - 80%

Answer 108

A

Short term ET intubation
Montgomery T-tube stenting for older child (4-6 weeks)
Distal tracheostomy (4-6 weeks)

Answer 109

A

Suprahyoid muscle release
Infrahyoid muscle release
Paratracheal ligament release
Intrapericardial hilar release
Dissection/release of pulmonary vasculature
Transplantation of L-mainstem bronchus
Neck flexion with chin-to chest suture (Grillo stitch)

Answer 110

A

Tracheal resection = for short segment stenosis
- Intermittent distal tracheal intubation

SIZES:
- < 2-3 cm resection = close without releasing maneuvers
- > 2-3cm resection = infrahyoid ± suprahyoid mobilization procedures

ADVANTAGES:
1. Epithelial lining present
2. Maintenance of cartilage contour

DISADVANTAGES:
1. Breakdown of anastomosis
2. Tracheal mobilization procedures risks blood supply and RLN

Vancouver 479

Answer 111

A

Slide Tracheoplasty:
- Typically for longer segment stenosis

Anesthetic considerations: Usually done with cardiopulmonary bypass

ADVANTAGES:
1. Epithelial lining present
2. Less mobilization compared to resection (Travel half the length of stenosis)
3. Doubles circumference

DISADVANTAGES:
1. Breakdown of anastomosis
2. Tracheal mobilization procedure risks blood supply and RLN

Vancouver 479

Answer 112

A

RLN damage
Granulation tissue
Infection
Dehiscence
Fistulization

Answer 113

A

Short term ETT
Montgomery t-tube stent x 4-6 weeks
Distal tracheostomy x 4-6 weeks

Answer 114

A

Tracheomalacia
Tracheal stenosis
Complete tracheal rings
Tracheal tumor/cyst
TEF
Pig bronchus (accessory bronchus originates directly from the supracarinal trachea)
External compression (e.g. vascular ring)
Infectious (tracheitis, croup)
Hemangioma
Tracheal agenesis (with a TEF)

Answer 115

A

Aka. PIG BRONCHUS

WHAT IS IT?
- Accessory bronchus originating directly from the supracarinal trachea (usually at a distance < 2cm from the carina)

INCIDENCE:
1. ~1%
2. Mostly on the right

COMPLICATIONS: (Mostly asymptomatic)
1. Occasional recurrent pneumonias due to focal emphysematous change

Vancouver 478

Answer 116

A

Preterm = 3.5mm
Term = 4.5-5mm

Failure to pass 4mm telescope = SGS

Estimate: Compare child’s pinky finger

Answer 117

A

A = pi * r ^2

75% reduction
16 fold increase in resistance

Adult:
Same degree of narrowing in adult = 30% reduction in diameter and doubles airway resistance

Answer 118

A

Smallest ETT that you can use and still ventilate safely
Treat LPR - PPI
Prolonged intubated up to 6 months has lESS risk than tracheostomy for SGS in infants
Prophylactic antibiotics at time of tracheostomy (prevents chondritis)

Answer 119

A

TYPES & CAUSES:

A. PRIMARY = CONGENITAL/INTRINSIC
1. Intrinsic deformity/weak cartilage
2. Absence of tracheal cartilage
3. Prematurity
4. Usually resolves as child grows

B. SECONDARY = CONGENITAL/EXTRINSIC
1. Extrinsic compression (e.g. vascular ring)

C. SECONDARY = ACQUIRED
1. Prolonged intubation
2. Iatrogenic: tracheostomy, CTR, TEF repair
3. Recurrent tracheitis –> leads to cartilage resorption
4. Relapsing polychondritis

CLINICAL PRESENTATION
1. Biphasic stridor or expiratory
2. “Washing machine” breathing on auscultation
3. Wheeze
4. Chronic barky cough
5. Frequent URTIs, exacerbated with infection
6. Failure to extubate
7. May persist with TEF fistula and large pouch

TREATMENT:
1. Primary intrinsic - usually resolves as child grows and cartilage stiffens (up to 4 years old)
2. Secondary extrinsic - relieve extrinsic compression
3. Secondary acquired - LTR, cap-graft

OPTIONS FOR MANAGEMENT:
1. Conservative/observation: Humidified air, chest physio, slow and careful feeding, reflux control
2. Non-invasive ventilation
3. Distal tracheomalacia: Aortopexy
4. Proximal/diffuse: Stenting or tracheostomy
5. Short segment stenosis (1-2 rings) - Tracheal resection
6. Long segment - Slide tracheoplasty

Answer 120

A

A. SILICONE TUBE STENT
Advantages:
1. Ease of removal
2. Less granuloma formation
3. Better for actively inflamed airway
4. More resistant to microbial colonization

Disadvantages:
1. Impairs mucociliary clearance
2. More likely to migrate
3. Does not conform as well
4. Thicker stent walls less practical in infants and small children

B. METALLIC MESH STENT
Advantages:
1. Ease of insertion
2. Can be placed via flexible bronchoscope in compressed state
3. Conforms better to different geometries
4. Mucociliary clearance preservation

Disadvantages:
1. Granulation tissue
2. Difficult to remove/reposition (epithelization occurs in 6-8 weeks)
3. Erosion

C. BIOABSORBABLE STENT

D. EXTRALUMINAL SPLINT

Answer 121

A

TYPES:
1. Aberrant innominate artery (most common anomaly, arises more medial than normal; anterior compression)
2. Double aortic arch (most common “vascular ring” - compresses both trachea and esophagus)
3. Right arch with ligamentum arteriosum
4. Aberrant right subclavian artery
5. Aberrant left pulmonary artery (Pulmonary sling)
6. Anomalous left carotid artery
7. PUlmonary artery dilation

CLINICAL PRESENTATION/SYMPTOMS:
1. Biphasic stridor
2. Wheeze
3. Barky cough
4. Frequent URTIs
5. Dysphagia (if esophagus involved)
6. Reflex apnea from vagal stimulation
7. “Dying spells” (apnea/cyanotic episodes) if severe
8. Purple spells (for pulmonary sling)

DIAGNOSIS/WORK-UP:
1. MRI
2. ECHO
3. Bronchoscopy - Pulsatile indentations of trachea/esophagus

SYNDROMES:
1. CHARGE
2. Velocardiofacial
3. Down Syndrome

Most common anomalies with VCF:
1. Innominate compression
2. Double aortic arch
3. Retroesophageal subclavial (dysphagia lusoria)

TREATMENT:
1. Consult cardiac surgery
2. Divide offending ligament/vessel & reanastamose to major vessel to relieve obstruction

Vancouver 480

https://my.clevelandclinic.org/-/scassets/images/org/health/articles/23947-vascular-rings

Answer 122

A

Most common vascular anomaly
Normal innominate = brachiocephalic trunk (right innominate artery)
Aberrant innominate artery = Innominate moves towards the left side of arch, then courses obliquely across trachea

Location of compression: High anterior trachea (just below thoracic inlet)
- R > L
- Pulsatile, could affect the right arm pulse

Normal innominate: https://upload.wikimedia.org/wikipedia/commons/thumb/e/e6/Gray506.svg/1200px-Gray506.svg.png
Aberrant innominate artery: https://www.researchgate.net/publication/365819831/figure/fig5/AS:11431281103424923@1669684244911/Innominate-artery-compression-syndrome-In-children-the-brachiocephalic-innominate.jpg

Answer 123

A

Most common vascular ring = double aortic arch
20% associated with 22q deletion
Ascending aorta bifurcates around trachea and esophagus, then rejoins the descending aorta

EMBRYOLOGY:
1. Normally the fourth branchial arch becomes the aorta on the left side and the innominate artery on the right side
2. The reason the 4th arch doesn’t become another paired aortic arch is because the posterior aspect of the 4th arch is supposed to involute to the right
3. Persistence of the posterior aspect = paired aorta = double aortic arch

Location of compression:
1. Anterior trachea
2. Posterior esophagus (causes dysphagia)

https://my.clevelandclinic.org/-/scassets/images/org/health/articles/23947-vascular-rings

Kevan Peds Question 162

Answer 124

A

Aortic arch takes off on the right side
Aberrant left subclavian takes off from right side of aortic arch, and is attached to the left pulmonary artery by ligamentum arteriosum forming a ring

Location of compression: posterior esophagus (no tracheal compression)

https://www.hawaii.edu/medicine/pediatrics/pedtext/s07c07fig2.jpg
Kevan Peds Question 162

Answer 125

A

Aortic arch forms in front of trachea/esophagus, then right subclavian passes behind the trachea/esophagus rather than in front (from the left)

Associations:
1. Dysphagia Lusoria (dysphagia secondary to aberrant right subclavian artery)
2. Non-recurrent right RLN
3. Situs inversus, dextrocardia

Location of compression: posterior esophagus (no tracheal compression)

https://www.researchgate.net/profile/Jaroslaw-Kasprzak/publication/264644130/figure/fig2/AS:1088646107144227@1636564866786/Schematic-arrangements-of-the-presence-of-an-aberrant-right-subclavian-artery.jpg

Answer 126

A

Pulmonary artery courses between trachea and esophagus

Airway associations:
1. Complete tracheal rings
2. Tracheomalacia (Type 2)
3. Distal tracheal stenosis

Location of compression:
1. Posterior trachea
2. Anterior esophagus

Vancouver 481

Normal pulmonary artery: https://cdn.britannica.com/20/125820-050-F1FD8A7E/veins-arteries-human.jpg
Aberrant left pulmonary artery/pulmonary sling: https://img.medscapestatic.com/pi/meds/ckb/09/42809tn.jpg

Answer 127

A

Double aortic arch
Right aortic arch

These two make up ~85-95% of all vascular rings

Answer 128

A

ABSOLUTE:
1. Reflex apnea (from vagal stimulation)
2. Failure of medical management of severe respiratory distress after 48 hours
3. Prolonged intubation

RELATIVE:
1. Repeated URTI episodes
2. Exercise intolerance
3. Significant FTT & dysphagia
4. Coexisting pathology (SGS, asthma, CF, or previous TEF repair)

Answer 129

A

GROSS CLASSIFICATION (VOGT CLASSIFICATION in brackets)

Gross Type A (Vogt II): Complete esophageal atresia, no fistula (8%)
Gross Type B (Vogt IIIa): Esophageal atresia + proximal TEF (1%)
Gross Type C (Vogt IIIb): Esophageal atresia + distal TEF (most common - 86%)
Gross Type D (Vogt IIIc): Esophageal atresia + proximal and distal TEFs (1%)
Gross Type E (Vogt “H-type”): No atresia, simply TEF (4%)

Vancouver 481

https://operativereview.com/wp-content/uploads/2022/09/Esophageal-Atresia-Types.jpg - Vogt type incorrect here

https://en.wikipedia.org/wiki/Tracheoesophageal_fistula

Answer 130

A

SYMPTOMS:
1. In utero: polyhydramnios (esophageal atresia)
Neonatal:
1. Feeding difficulty
2. Aspiration
3. Pneumonia
4. Respiratory distress
5. Excessive mucous
6. Esophageal atresia with TEF: Enlarged abdomen, air in stomach/bowel
7. Esophageal atresia without TEF: Scaphoid abdomen, no air in stomach/bowel

WORK-UP and DIAGNOSIS:
1. Failure to pass NG > 10cm
2. XR: NG curled in pharynx/thorax
3. Endoscopy

ASSOCIATIONS:
1. VACTERL
2. Trisomy 21
3. Trisomy 18
4. 22q deletion
5. CHARGE

TREATMENT:
1. Surgical repair
2. Dilatations of strictures

Answer 131

A

After TEF repair, can be left with a pouch. If intubating (later), ETT can get stuck in the pouch.
Therefore - pull back a few mm’s!

“They’re intubated, why are they crashing?”

Answer 132

A

Leak
Secondary fistula
Laryngeal cleft

Answer 133

A

V: Vertebral/Vascular anomalies
A: Anal atresia
C: Cardiac anomalies (PDA, valve problems)
TE: Tracheoesophageal fistula
R: Renal/radial bone anomalies
L: Limb anomalies (extra digits, shortened limbs)

Answer 134

A

Prolonged intubation
Emergent acute upper airway obstruction, unable to intubate (e.g. infections, trauma, etc.)
Fixed/chronic upper airway obstruction (e.g. hemangioma, cyst, neoplasm, VCP, craniofacial/syndrome)
Neurologic/muscular dysfunction
Pulmonary toilet
Secretion management
Facilitate major H&N surgery

Kevan Pediatric Question 168 (Table 92.1)

Answer 135

A

Neck extended with shoulder roll
Place ETT first
Keep NG in situ to prevent mistaking esophagus for trachea
Vertical incision
Maturation sutures on stoma
De-fat
Stay sutures through cartilage ring on each side of tracheal incision, secured to skin
Do not close skin incision to avoid subcutaneous emphysema
CXR in PACU to r/o pneumothorax and verify tube position
Post-op: Keep neck in flexion
Post-op: Antibiotics to prevent chondritis –> SGS/tracheomalacia
ICU monitoring post-op
Tracheostomy set at bedside always, hemostat, suction, same trach tube and one size smaller
Tracheostomy change at day 5-7

Answer 136

A

INTRAOPERATIVE COMPLICATIONS:
1. bleeding
2. Loss of airway/inability to ventilate
3. Subcutaneous emphysema
4. Pneumomediastinum
5. Pneumothorax
6. Esophageal injury
7. Creation of false passage
8. Recurrent laryngeal nerve injury
9. Cardiopulmonary arrest
10. Death
11. Damage to surrounding structures: Carotid, innominate, IJV, RLN, esophagus, thymus, larynx, posterior tracheal wall, lung

EARLY POST-OPERATIVE COMPLICATIONS (< 7 days)
1. Accidental decannulation
2. Tracheostomy tube occlusion
3. Bleeding
4. Subcutaneous emphysema
5. Pneumomediastinum
6. Pneumothorax
7. Creation of false passage
8. Stoma/wound breakdown or cellulitis
9. Neck skin erosion from tracheostomy tube ties
10. Tracheitis

LATE POST-OPERATIVE COMPLICATIONS (> 7 days)
1. Accidental decannulation
2. Tracheostomy tube occlusion
3. Peristomal granulation tissue
4. Suprastomal granulation tissue
5. Stoma/wound breakdown or cellulitis
6. Neck skin erosion from tracheostomy tube ties
7. Tracheostomy stomal stenosis
8. Suprastomal cartilaginous collapse
9. Subglottic stenosis
10. Tracheomalacia
11. Tracheitis
12. Tracheal stenosis
13. Tracheal granulation tissue
14. Airway hemorrhage
15. Tracheo-innominate artery fistula
16. Persistent tracheocutaneous fistula after decannulation
17. Erosion into surrounding structures (e.g. mediastinum, esophagus, innominate)

Answer 137

A

Use a 12-14 G needle catheter to ventilate
Ventilate 1 second inspiration, 4 second expiration
Can sustain up to 30 minutes before CO2 accumulates

Answer 138

A

Neonates/Infants = 6 months (softer tissues, greater risk from actual tracheostomy than from prolonged ETT)

Children = 50 days

Adults = 7-10 days

Answer 139

A

Expressive
Non-vocal behaviour
If air leak - passy muir valve

AVOID fenestrated tubes (suprastomal granulation more common!)

Answer 140

A

TRACHEOSTOMY

Advantages:
1. Shorter, larger tube can be placed
2. Decreased airway dead space
3. Less damage to larynx, including supraglottic, glottic, and subglottic regions
4. More comfortable for the patient
5. May allow child to be discharged from the hospital, even on a ventilator
6. Care for the tracheostomy can be performed by trained caregivers/family who are not health care professionals

Disadvantages:
1. Requires an experienced surgeon
2. Complications associated with tracheostomy
3. Requires a surgical procedure

PROLONGED INTUBATION

Advantages:
1. Can be performed by a variety of health care providers
2. Does not require a surgical procedure and associated complications

Disadvantages:
1. Endotracheal tubes may be plugged easily
2. Increased airway dead space
3. More likely to cause damage to larynx and trachea
4. Less comfortable for patient
5. Care cannot be performed easily by patient/family caregivers

Answer 141

A

Patient tolerates tracheostomy tube downsizing
Patient is able to use tracheostomy cap for all waking hours
Patient successfully completes a 48 hour capping period while admitted to the hospital for observation
Direct laryngoscopy and bronchoscopy rules out any anomaly in the patient that would preclude decannulation
Patient completes a capped tracheostomy sleep study with favourable results (AHI < 10, obstructive index < 5, end tidal CO2 > 50mmHg for less than 25% of sleep time)

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Airway Pathology (not sleep) - Stridor, RRP, infections Flashcards

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