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

Question

What is the differential diagnosis of congenital supraglottic abnormalities? 8

Answer 1

1. Laryngomalacia 2. Hemangioma 3. Lymphatic malformation 4. Laryngocele 5. Saccular cyst 6. Anomalous cuneiform cartilage (4th arch) 7. Bifid epiglottis 8. Supraglottic web

Answer 2

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

Answer 3

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

Answer 4

Bronchoscopy r/o subglottic stenosis

Answer 5

1. Non-infective barky ough 2. 1-3 year olds 3. Normal during the day, worse at night ± stridor

Answer 6

Clinical: Palpate in OR - hemangioma is compressible Imaging: MRA

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

1. Chemical epiglottitis 2. Inhalational/thermal injury 3. Angioedema/allergy 4. Trauma 5. Sarcoid

Answer 11

1. Angioneurotic edema 2. Allergic reaction 3. Trauma 4. Candida infection 5. AE fold cyst 6. Sarcoid 7. Corrosive ingestion 8. Lymphovascular malformation

Answer 12

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

Answer 13

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

Answer 14

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 ## Footnote Kevan Peds Question 108##

Answer 15

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

Answer 16

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

Answer 17

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 ## Footnote 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

Answer 18

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

Answer 19

1. Airway obstruction (from tonsillar enlargement) 2. Splenomegaly/rupture (avoid contact sports x 6 months) 3. Hepatitis 4. CNS: meningitis, encephalitis, transverse myelitis 5. Guillain-Barre, cranial neuropathies (esp. CN7) 6. Hemolytic anemia 7. Myocarditis CASHH MG

Answer 20

Culture from swab of ulcer demonstrating multinucleated cells seen on Tzanck smear ## Footnote Kevan Gen #55

Answer 21

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 ## Footnote Kevan Peds Question 110 Cummings chapter 201 Table 201.1

Answer 22

1. Single dose Ceftriaxone / Cefixime 2. Always empirically treat concomitant chlamydia (single dose Azithromycin, or Doxycycline x 7 days) Even if asymptomatic --> highly contagious

Answer 23

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

Answer 24

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

Answer 25

1. Epstein Barr Virus (mononucleosis) 2. Group A beta-hemolytic Streptococcus 3. Corynebacterium DIphtheriae 4. Neisseria Gonorrhaea 5. Syphillis 6. Vincent's angina: Acute necrotizing/ulcerating gingivitis/oral infection - gram-negative Fusiformis ("trench mouth") 7. Candidiasis (Albicans)

Answer 26

1. Viral presence in nasal cavity --> inflammatory reaction (NOT invasion) of nasal epithelium --> mucosal edema/hyperemia --> extends down into pharynx Usually self-limited

Answer 27

1. Laryngomalacia 2. Vocal fold paralysis 3. Subglottic stenosis

Answer 28

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

Answer 29

Laryngomalacia

Answer 30

Laryngomalacia

Answer 31

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%) SPIRA

Answer 32

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

Answer 33

OLNEY CLASSIFICATION (1999): 1. Type 1: Anterior collapse of arytenoids 2. Type 2: Shortened aryepiglottic folds 3. Type 3: Prolapsed 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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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"

Answer 38

- 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

Answer 39

- 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)

Answer 40

1. Chronic cough 2. Hoarseness 3. Aspiration 4. Recurrent croup 5. Laryngomalacia 6. Episodic laryngospasm 7. Subglottic stenosis "CHARLES"

Answer 41

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

Answer 42

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)

Answer 43

1. Spontaneous ventilation (most common) 2. Supplemental blow-by oxygen via NG 3. O2 via bronchoscopy 4. Jet ventilation 5. Intermittent BMV 6. Intermittent intubation 7. 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

Answer 44

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 (bilateral) 1. Idiopathic 2. Arnold Chiari malformation 3. Birth trauma

Answer 45

1. Idiopathic 2. Birth trauma 3. Arnold Chiari 4. Increased ICP (e.g. hydrocephalus) 5. Neuropathy of prematurity

Answer 46

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 47

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 48

*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 ## Footnote Vancouver 472

Answer 49

1. 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 2. 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 3. Type III: Herniation of cerebellum (high cervical meningocele) - Rare 4. Type IV: Cerebellar Hypoplasia (Dandy-Walker Syndrome) - Rare

Answer 50

1. CN IX-XII difficulties 2. Bilateral vocal fold paralysis, Respiratory distress 3. Poor feeding 4. Aspiration

Answer 51

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 52

Laryngeal webs are on the sepctrum of laryngeal atresia Types: 1. Glottic (anterior & posterior): 75% 2. Subglottic < 10% 3. Supraglottic < 5%

Answer 53

1. Flexible laryngoscopy 2. ± Rigid laryngoscopy + bronchoscopy (site, thickness, horizontal and vertical extent) 3. ± X-ray (Sail sign = persistent tissue between Vocal cords and subglottis, rule out SGS) 4. ± FISH for anterior glottic web (22q11.2 deletion)

Answer 54

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

Answer 55

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 56

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 ## Footnote Kevan Pediatrics Question 146

Answer 57

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

Answer 58

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 ## Footnote Vancouver 476

Answer 59

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 60

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 DIAGNOSIS: 1. Laryngoscopy with palpation 2. BAL to look for lipid-laden macrophages (for signs of aspiration) 3. Modified Barium swallow (r/o aspiration) 4. CXR (chronic aspiration/pneumonia) 5. Flexible fiberoptic laryngoscopy & FEES TREATMENT 1. Conservative - PT/OT/SLP: Behavioural modifications - Thickened feeds - PPI 2. 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) ## Footnote Vancouver 477

Answer 61

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

Answer 62

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 63

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 ## Footnote Vancouver 477

Answer 64

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 ## Footnote Vancouver 478

Answer 65

1. Thyroid function tests (Bamforth syndrome) 2. Pituitary work up (Pallister hall syndrome)

Answer 66

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

Answer 67

1. All girls and boys ages 11-12 (Grade 6) 2. Catch up vaccine - Girls 13-26 years of age - Boys 13-21 years of age

Answer 68

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 ## Footnote Chapter 208 Fig 208.1

Answer 69

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 70

30% children 15% adult

Answer 71

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 72

1. No aerosolization of HPV virus 2. Quicker set up 3. No thermal injury 4. Lower cost 5. No risk of airway fire 6. Better voice outcomes (controversial)

Answer 73

1. HPV Type 16, 18 2. Smoking 3. Radiotherapy in childhood

Answer 74

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 75

- 4.5-5mm in diameter - 3-4mm in premature - Size 3 ETT SGS at term = < 4mm Premature = < 3mm

Answer 76

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 77

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

Answer 78

1. Soft tissue (granulation tissue, submucosal gland hyperplasia, submucosal fibrosis) 2. Cartilaginous, normal shape (Cricoid small for infant's size) 3. Cartilaginous, abnormal shape (Elliptical, large anterior lamina, large posterior lamina, generalized thickening, submucous/incomplete laryngeal cleft, other) 4. Cartilaginous (trapped first tracheal ring) 5. Combined stenosis

Answer 79

- 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 80

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 81

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 82

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 5. Positive pressure ventilation (e.g. CPAP/BIPAP) - for temporizing measures before securing airway

Answer 83

C. SURGICAL OPTIONS 1. Tracheostomy 2. Balloon dilations - Only good for early soft tissue stenosis - ± Mitomycin C injection - ± Steroid injection 3. Endoscopic CO2 laser OR cold steel - CO2 only good for small, isolated scar bands 4. 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) 5. Posterior Cricoid split ± cartilage graft 6. Four Quadrant technique 7. LTR/LTP (see other card) 8. Slide tracheoplasty (see other card) 9. Cricotracheal resection (see other card)

Answer 84

"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: 1. Circumferential cicatricial scarring 2. Abundant scar tissue >1cm in the vertical dimension 3. Fibrotic scar tissue in the interarytenoid area of the posterior commissure 4. Cartilaginous stenosis 5. Loss of cartilaginous framework 6. Infection of trachea after tracheotomy 7. Exposure of perichondrium or cartilage during CO2 laser excision, predisposing to perichondritis and chondritis 8. Combined laryngo-tracheal stenosis 9. Concomitant tracheal disease 10. Previous endoscopic management failure FAIL CAT Failure - previous endoscopic management failure Abundant scar tissue >1cm in vertical dimension Infection of the trachea/cartilage Loss of cartilaginous framework (e.g. fracture, etc.) Cartilage or perichondrium exposure during laser excision, predisposing to perichondritis and chondritis Arytenoid (interarytenoid) area at the posterior commissure ++ fibrotic scar tissue Tracheal disease concomitant or combined laryngo-tracheal stenosis Laryngology: CLIPPINGS: Circumferential thick (cicatricial) scarring Length >1 cm Involved/Exposure of cartilage during CO2 laser excision predisposing to chondritis Posterior glottic stenosis with arytenoid fixation Previous failure Infection associated with tracheostomy (either current or previous) ("Not enough") Loss of cartilaginous framework Glottic involvement Stenosis of the trachea/concomittant laryngo/tracheal diseases

Answer 85

1. Laryngeal mask airway 2. Heliox 3. Spontaneous breathing (induction via inhalational mask, then TIVA anesthetic) 4. Intermittent extubation 5. Jet ventilation (adults only?) 6. THRIVE - Transnasal Humidified Rapid-Insufflation Ventilatory Exchange

Answer 86

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 87

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

Answer 88

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

Answer 89

CAUSES: 1. Primary: Complete tracheal rings, Down's syndrome, Pfeiffer syndrome 2. Secondary: similar to SGS 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 ## Footnote 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 90

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

Answer 91

Indications: 1. > 10kg 2. Grade 1-4 stenosis 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) 6. Significant cricoid deformity "PCS" 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) ## Footnote See Half day lecture on airway anomalies for images

Answer 92

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)

Answer 93

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

Answer 94

1. Posterior glottic/subglottic stenosis 2. Complete glottic/subglottic stenosis 3. Significant cricoid deformity "PCS = Posterior cricoid split"

Answer 95

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 96

1. Grade III and IV 2. 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 97

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 98

1. Short term ET intubation 2. Montgomery T-tube stenting for older child (4-6 weeks) 3. Distal tracheostomy (4-6 weeks)

Answer 99

1. Suprahyoid muscle release 2. Infrahyoid muscle release 3. Paratracheal ligament release 4. Intrapericardial hilar release 5. Dissection/release of pulmonary vasculature 6. Transplantation of L-mainstem bronchus 7. Neck flexion with chin-to chest suture (Grillo stitch) "DINT SIP"

Answer 100

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 ## Footnote Vancouver 479

Answer 101

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 ## Footnote Vancouver 479

Answer 102

1. RLN damage 2. Granulation tissue 3. Infection 4. Dehiscence 5. Fistulization

Answer 103

1. Short term ETT 2. Montgomery t-tube stent x 4-6 weeks 3. Distal tracheostomy x 4-6 weeks

Answer 104

1. Tracheomalacia 2. Tracheal stenosis 3. Complete tracheal rings 4. Tracheal tumor/cyst 5. TEF 6. Pig bronchus (accessory bronchus originates directly from the supracarinal trachea) 7. External compression (e.g. vascular ring) 8. Infectious (tracheitis, croup) 9. Hemangioma 10. Tracheal agenesis (with a TEF)

Answer 105

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 ## Footnote Vancouver 478

Answer 106

Preterm = 3.5mm Term = 4.5-5mm Failure to pass 4mm telescope = SGS Estimate: Compare child's pinky finger

Answer 107

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 108

1. Smallest ETT that you can use and still ventilate safely 2. Treat LPR - PPI 3. Prolonged intubated up to 6 months has LESS risk than tracheostomy for SGS in infants 4. Prophylactic antibiotics at time of tracheostomy (prevents chondritis)

Answer 109

TYPES & CAUSES: A. PRIMARY = CONGENITAL/INTRINSIC 1. Intrinsic deformity/weak cartilage 2. Absence of tracheal cartilage 3. Prematurity - 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

Answer 110

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 DIAGNOSIS 1. Bronchoscopy 2. Dynamic CT 3. Echo (or MRI) if identified to rule out vascular ring 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 111

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 112

CLINICAL PRESENTATION/SYMPTOMS: - similar to tracheomalacia 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 TREATMENT: 1. Consult cardiac surgery 2. Divide offending ligament/vessel & reanastamose to major vessel to relieve obstruction ## Footnote Vancouver 480 https://my.clevelandclinic.org/-/scassets/images/org/health/articles/23947-vascular-rings

Answer 113

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

Answer 114

SYNDROMES: "CVD" think cardiovascular disease 1. CHARGE 2. Velocardiofacial 3. Down Syndrome Most common anomalies with VCF: 1. Innominate compression 2. Double aortic arch 3. Retroesophageal subclavial (dysphagia lusoria)

Answer 115

- 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 ## Footnote 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 116

- 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) ## Footnote https://my.clevelandclinic.org/-/scassets/images/org/health/articles/23947-vascular-rings Kevan Peds Question 162

Answer 117

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

Answer 118

- 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) ## Footnote 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 119

- Left Pulmonary artery courses between trachea and esophagus (first a main trunk goes to the right side, and then the left pulmonary artery takes off late and goes in between the two) Airway associations: 1. Complete tracheal rings 2. Tracheomalacia (Type 2) 3. Distal tracheal stenosis Location of compression: 1. Posterior trachea 2. Anterior esophagus ## Footnote 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 120

1. Double aortic arch 2. Right aortic arch These two make up ~85-95% of all vascular rings

Answer 121

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 122

GROSS CLASSIFICATION (VOGT CLASSIFICATION in brackets) 1. Gross Type A (Vogt II): Complete esophageal atresia, no fistula (8%) 2. Gross Type B (Vogt IIIa): Esophageal atresia + proximal TEF (1%) 3. Gross Type C (Vogt IIIb): Esophageal atresia + distal TEF (most common - 86%) 4. Gross Type D (Vogt IIIc): Esophageal atresia + proximal and distal TEFs (1%) 5. Gross Type E (Vogt "H-type"): No atresia, simply TEF (4%) ## Footnote 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 123

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 124

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 125

1. Leak 2. Secondary fistula 3. Laryngeal cleft

Answer 126

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 127

1. Prolonged intubation 2. Emergent acute upper airway obstruction, unable to intubate (e.g. infections, trauma, etc.) 3. Fixed/chronic upper airway obstruction (e.g. hemangioma, cyst, neoplasm, VCP, craniofacial/syndrome) 4. Neurologic/muscular dysfunction 5. Pulmonary toilet 6. Secretion management 7. Facilitate major H&N surgery Basically similar indications to adults ## Footnote Kevan Pediatric Question 168 (Table 92.1)

Answer 128

1. Neck extended with shoulder roll 2. Place ETT first 3. Keep NG in situ to prevent mistaking esophagus for trachea 4. Vertical incision 5. Bjork flap 5. Maturation sutures on stoma 6. De-fat 7. Stay sutures through cartilage ring on each side of tracheal incision, secured to skin 7. Do not close skin incision to avoid subcutaneous emphysema Post-op: 8. CXR in PACU to r/o pneumothorax and verify tube position 9. Post-op: Keep neck in flexion 10. Post-op: Antibiotics to prevent chondritis --> SGS/tracheomalacia 11. ICU monitoring post-op 12. Tracheostomy set at bedside always, hemostat, suction, same trach tube and one size smaller 13. Tracheostomy change at day 5-7

Answer 129

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 130

1. Use a 12-14 G needle catheter to ventilate 2. Ventilate 1 second inspiration, 4 second expiration 3. Can sustain up to 30 minutes before CO2 accumulates

Answer 131

Neonates/Infants = 6 months (softer tissues, greater risk from actual tracheostomy than from prolonged ETT) Children = 50 days Adults = 7-10 days

Answer 132

1. Expressive 2. Non-vocal behaviour 3. If air leak - passy muir valve AVOID fenestrated tubes (suprastomal granulation more common!)

Answer 133

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 134

1. Patient tolerates tracheostomy tube downsizing 2. Patient is able to use tracheostomy cap for all waking hours 3. Patient successfully completes a 48 hour capping period while admitted to the hospital for observation 4. Direct laryngoscopy and bronchoscopy rules out any anomaly in the patient that would preclude decannulation 5. 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)

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

(161 cards)