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Diplomate exam > Laryngology And Bronchoesophagology > Flashcards

Laryngology And Bronchoesophagology Flashcards

1
Q

Mc cause of stridor in infants?

A

Laryngomalacia

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2
Q

Noniatrogenic neonatal unilateral and bilateral vocal cord paralysis will resolve spontaneously in ___ of patients?

A

50%

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3
Q

All these children should undergo genetic testing for abnormalities in chromosome 22q11?

A

With congenital anterior laryngeal webs

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4
Q

Often present with history if recurrent croup with improvement with steroids?

A

Subglottic hemangioma

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5
Q

Noisy breathing from the vibration of tissues above level of the larynx?

A

Stertor

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6
Q

Hallmark of laryngeal obstruction described as a high pitched, musical or harsh sound often mistaken for wheezing.

A

Stridor

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7
Q

Stridor that results from glottic obstruction presents on?

A

Inspiration

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8
Q

Obstruction at or below level of the glottis, in subglottis and upper trachea?

A

Biphasic stridor

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9
Q

Expiratory stridor results from lesions of the?

A

Distal trachea or mainstem bronchi

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10
Q

Hallmark symptom which leads to airway evaluation?

A

Noisy breathing

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11
Q

Can give this as an intralesional injection in papillomatosis?

A

Cidofovir injection

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12
Q

Presentation of infant with laryngomalacia?
Median resolution time?
By what age will the vast majority have no more stridor?

A

Intermittent inspiratory stridor within the first 2 weeks of life, resolves slowly over several months.

7-9 mos

By 18 mos of age

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13
Q

What is the relation of LM to crying?

A

Mild LM - improves with crying
Moderate-Severe LM - stridor will worsen with crying because of the increased airflow through the severely collapsed larynx

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14
Q

Anatomic anomaly in severe LM?

A

Shorter aryepiglottic fold

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15
Q

Optimal way to diagnose LM?

A

Fiberoptic flexible laryngoscopy in the awake patient

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16
Q

Co morbid disease with LM?

A

GERD

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17
Q

What are the various anatomic abnormalities that lead to supraglottic obstruction in patients with LM?

A
  • Anterior prolapse of mucosa overlying arytenoid cartilage (57%)
  • Short aryepiglottic fold that tether the epiglottis posteriorly (15%)
  • Posterior collapse of the epiglottis (12%)
  • Combination (15%)
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18
Q

What is the simplest type of supraglottoplasty?

A

Division of the short aryepiglottic folds

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19
Q

How to avoid post operative stenosis after supraglottoplasty?

A

Preserve interarytenoid mucosa

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20
Q

Incidence of RLN injury in patent ductus arteriosus ligation cases?

A

1-7.4%

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21
Q

How to best dx VFP?

A

FFL (awake)

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22
Q

_____ of noniatrogenic unilateral VFP wil resolve spontaneously mostly within the first _____ of life.

A

70%

6 mos.

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23
Q

Classic presentation of a patient with paradoxic vocal fold motion?

A

Episodic stridor that is loud and high pitched, interspersed with periods of normal breathing

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24
Q 
What is the glottic web classification by Cohen?
Severity
Extent of glottic obstruction
Subglottic involvement
Symptoms
A

Type 1,<35%,none or little, mild hoarseness

Type 2, 35-50%, thin anterior web with little subglottic extension, hoarse weak cry,stridor with exertion

Type 3, 50-75%, thin-thick web, extends to lower border of cricoid, severe hoarseness, moderate airway obstruction

Type 4, 75-90%, thick web, extends to lower cricoid, aphonic, severe airway obstruction, requires tracheotomy

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25
Q

In addition to chromosome abnormalities, laryngeal webs are also associated with?

A

Cardiac abnormalities (particular attention to aortic arch)

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26
Q

What is the most severe form if laryngeal web?

A

Total atresia of the larynx

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27
Q

What is the definition of subglottic stenosis in a term newborn?

A

Cricoid diameter of less than 3.5mm

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28
Q

What is malformed in congenital stenosis?

A

Cricoid cartilage

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29
Q

What is the anatomic abnormality in congenital subglottic stenosis?

A

Elliptical cricoid cartilage (transverse diameter is smaller than AP diameter) (normal is equal at inferior border of cricoid cartilage)

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30
Q

Elliptical cricoid may be found in association with?

A

Laryngeal cleft

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31
Q

Benign vascular malformations associated with immaturity?

A

Subglottic infantile hemangiomas

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32
Q

Incidence of subglottic IH?

A

Female:male 2:1

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33
Q

Histopathology of IH?

A

Endothelial proliferation and uniform, strongly positive staining for erythrocyte-type GLUT-1.

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34
Q

Cutaneous IH in “beard distribution” associated with airway IH in ____ of cases.

A

50%

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35
Q

Traditional medical treatment of subglottic hemangioma?

A

Systemic steroids

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36
Q

Average time to decannulation in an infant ff tracheostomy for subglottic IH?

A

27 months following tracheotomy

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37
Q

Mortality rate of tracheostomy in an infant?

A

1-2%

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38
Q

Most significant complication associated with laser treatment?

A

Subglottic stenosis in 18% of cases

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39
Q

What dosage of propanolol is initiated in subglottic IH?

A

0.33 mg/kg/dose (or 1mg/kg/day divided in 3 doses daily), escalating to a maximum of 2-3mg/kg/day divided into 3 doses daily. Give dose with meals

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40
Q

When is inpatient admission advised for propanolol treatment for subglottic IH?

A

Infants 8 weeks of gestationally corrected age or younger

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41
Q

Treatment duration of propanolol therapy for subglottic IH?

A

4-12mos

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42
Q

Cause of subglottic cysts?

A

Intubation trauma

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43
Q

Lining of vallecular cysts?

A

Pseudostratified ciliated or squamous epithelium of thyroglossal duct origin

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44
Q

Mc presenting symptom of vallecular cyst?

A

Stridor

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45
Q

Gold standard for diagnosis of vallecular cyst?

A

Flexible or direct laryngoscopy

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46
Q

What is the laryngeal saccule?

A

A pouch of mucous membrane from the anterior-superior portion of the laryngeal ventricle.

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47
Q

Abnormal dilation or herniation of the saccule that may be internal, external, or a combination?

A

Laryngocele

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48
Q

What is an internal laryngocele?

A

Confined to the interior of the larynx and extend posterosuperiorly into the area of the FVF and aryepiglottic fold

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49
Q

What is an external laryngocele?

A

Passes through the thyrohyoid membrane and presents as a mass in the neck.

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50
Q

What are saccular cysts?

A

Result from obstruction of the laryngeal saccule orifice or the collecting ducts of the submucosal glands located around the ventricle

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51
Q

What is an anterior saccular cyst?

A

Protruding between the anterior and posterior vocal cords

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52
Q

What is a lateral saccular cyst?

A

Extends into the false vocal cord and aryepiglottic fold

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53
Q

Laryngoceles produce ___________ because of episodic filling with air, saccular cysts produce ___________ symptoms because of mucoid fluid within the cyst.

A

Intermittent upper airway obstruction and hoarseness

Constant

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54
Q

What is the cause of laryngeal cleft?

A

Failure of fusion of posterior cricoid lamina, which leads to abnormal communication between the posterior portion if the larynx and esophagus.

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55
Q

Whats the cause of laryngotracheoesophageal clefts?

A

Results from extension of a laryngeal cleft to involve incomplete development of the tracheoesophageal septum, leading to abnormal communication between the trachea and esophagus

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56
Q

MC classification system for laryngeal cleft based on vertical length of the cleft?

A

Benjamin-Inglis system

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57
Q

Submucous laryngeal cleft consists of?

A

A posterior midline cartilage defect with intact soft tissue that includes mucosa and interarytenoid muscle

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58
Q

MC congenital abnormality that accompanies LC and LTEC?

A

TEF and esophageal atresia

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59
Q

What is the benjamin inglis classification system for laryngeal clefts?

A 
Cleft location
Type 1 - interarytenoid
Type 2 - partial/complete cricoid
Type 3 - into cervical trachea
Type 4 - to intrathoracic trachea/carina
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60
Q

What is the Myer-Cotton classification of clefts?

A 
LI : interarytenoid
LII : partial cricoid
LIII : complete cricoid
LTEI : into cervical trachea
LTEII : to intrathoracic trachea/carina
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61
Q

Management for Type I LC?

A

Medical management

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62
Q

What is a bifid epiglottis?

A

Cleft of the epiglottis that encompasses at least 2/3 its length

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63
Q

Bifid epiglottis is associated with what other anomalies?

A 
Polydactyly (75%)
Cleft palate
Bifid uvula
Micrognathia
Microglossia
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64
Q

Another name for Pallister-Hall syndrome (PHS)?

A

Congenital hypothalamic hamartoblastoma syndrome

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65
Q

What characterizes pallister hall syndrome?

A

Polydactyly
Pituitary dysfunction
Imperforate anus
Laryngotracheal cleft

(Commonly associated with bifid epiglottis)

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66
Q

All patients with PHS (AD) have a high incidence of?

A

Hypothalamic and pituitary problems

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67
Q

2nd most common cause of congenital stridor in children and represents 10% of congenital anomalies of the larynx?

A

Vocal fold paralysis

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68
Q

What percentage of vocal fold paralysis in children is bilateral?

A

50%

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69
Q

What is the most specific and sensitive test to determine the presence of vocal fold paralysis?

A

Laryngeal electromyography (EMG)

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70
Q

Spontaneous recovery of vocal fold function may be possible after how many years?

A

2-3 years

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71
Q

What is the waiting period to perform surgery to permit decannulation of the child?

A

10-12months

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72
Q

What is the pathogenesis of laryngeal web?

A

The epithelium, which temporarily obliterates the developing laryngotracheal lumen and fails to reabsorb during the eighth week of embryogenesis.

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73
Q

Classification of Glottic webs?

A

Type 1: anterior web that involves 35% or less of the glottis. (Voice dysfunction)

Type 2: anterior web involves 50% of the glottis. (Voice disorder)

Type 3: involves 75% of the glottis, and anterior portion of the web is solid and extends into the subglottis

Type 4: involves 90% of the glottis, and the web is uniformly thick and extends into the subglottic area with resulting subglottic stenosis

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74
Q

Cause of posterior glottic stenosis?

A

From airway trauma from intubation

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75
Q

Types of posterior glottic stenosis?

A

Type 1: vocal process adhesion

Type 2: posterior commissure or interarytenoid scar

Type 3: congenital or acquired unilateral cricoarytenoid fixation with or without interarytenoid scar

Type 4: congenital or acquired bilateral cricoarytenoid fixation with or without interarytenoid scar

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76
Q

Presenting symptom in patients with interarytenoid web and scarring? (Abduction is impaired but adduction is normal)

A

Airway compromise

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77
Q

Most common benign neoplasm of the larynx?

A

Recurrent respiratory papillomatosis

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78
Q

Where do papillomas have a predilection for?

A

Anatomic sites where ciliated and squamous epithelia are juxtaposed

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79
Q

Common sites of RRP in larynx?

A
  • Midzobe of the laryngeal surface of epiglottis
  • Upper and lower margins of the ventricles
  • Undersurface of the vocal folds
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80
Q

RRP is first diagnosed in patients?

A

Between the ages of 2 and 3 years

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81
Q

Association between what types of hpv in RRP?

A

Hpv types 6 and 11. HPV found in genital tract of 25% of women of child bearing age and is clinically apparent jn 2-5%

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82
Q

Goal of surgery in RRP?

A

Establish a stable airway and a serviceable voice

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83
Q

Surgical removal of papillomas are until what level?

A

Level of the mucosa or submucosa, (avoiding deeper muscular and ligamentous levels)

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84
Q

Incidence of spontaneous malignant degeneration of longstanding RRP?

A

2-3%

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85
Q

Pathogenesis of granuloma?

A

Intubation trauma

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86
Q

Most reliable means of diagnosing GERD?

A

Prolonged (24 hr) pH manometry study

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87
Q

What is a reflux event?

A

Drop in pH to less than 4

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88
Q

What is the pathogenesis of vocal nodules?

A

From mechanical trauma and occur at the free edge of the anterior and middle third of the vocal fold

89
Q

What are the 3 stages of the development of vocal fold nodules?

A
  1. Inflammatory phase with increased vascularity and protein accumulation
  2. Localized swelling on the edge of the vocal fold that appears as grayish, translucent thickening (nodules are reversible within 24-48hrs it trauma is eliminated)
  3. Replacement of thickening by fibrotic tissue that appears gray or white
90
Q

What is the histologic picture of vocal fold nodules?

A

Circumscribed hyperplasia or hyperkeratinization and secondary hyaline degeneration in the lamina propria

91
Q

What is the etiologic agent for RRP?

A

Hpv 6 and 11

92
Q

Histologic characteristic of RRP?

A

Proliferation of benign squamous papillomas within the aerodigestive tract

93
Q

Most common benign neoplasm of the larynx among children and the 2nd most common cause of childhood hoarseness?

A

RRP

94
Q

Most common site of involvement of RRP?

A

Larynx

95
Q

2 forms of RRP?

A
  1. Juvenile/Aggressive form

2. Adult/less aggressive

96
Q

What age of diagnosis of rrp portends a poorer prognosis?

A

Less than 3 years old

97
Q

What is the virology of hpv?

A

Belongs to the papovaviridae family, a small DNA-containing, non enveloped, icosahedral, capsid virus with a double stranded circular dna that is 7900 base pairs long. Hpv is epitheliotropic and infects epithelial cells.

98
Q

What hpv group is believed to have a low malignant potential?

A

Hpvs 6 and 11

99
Q

What hpv group is associated with malignancies in the genital and aerodigestive tract?

A

Hpv 18

100
Q

What layer does hpv affect?

A

Stem cells within the basal layer of mucosa

101
Q

What are the 3 regions of the viral genome? (Hpv)

A

Upstream regulatory region and 2 regions named according to the phase of the infcthon in which they are expressed - early (E) and late (L)

102
Q

What is a fundamental property of hpv?

A

Induction of cellular proliferation

103
Q

Histologic appearance of hpv?

A

This mucosal proliferation results in multiple “fronds” or fingerlike projections with a central fibrovascular core covered by stratified squamous epithelium.

RRP exhibits delayed maturation of the epithelium and results in a significantly thickened basal cell layer and nucleated cells in the superficial layers

104
Q

What are the gene products of hpv?

A

E6, E7 and possibly E5

105
Q

Most common manifestation of genital hpv?

A

Condylomata acuminata that involve the cervix, vulva or other anogenital sites

106
Q

Hpv is present in the genital tract of _____ of all women of childbearing age worldwide.

A

25%

107
Q

The first and predominant site of vocal fold lesions?

Second clinical symptom to develop?

A

Vocal fold - thus hoarseness is the principal presenting symptom in RRP

Stridor - initially inspiratory and becomes biphasic with progression of the disease

108
Q

Extralaryngeal spread of RRP has been identified in ____ of children and ____ of adults.

A

30%, 16%

109
Q

What are the most frequent sites of extralaryngeal spread (in decreasing order of frequency)?

A

Oral cavity
Trachea
Bronchi

110
Q

How do pulmonary lesions in RRP appear?

A

Asymptomatic noncalcified peripheral nodules

111
Q

Reason for respiratory failure in RRP?

A

Destruction of lung parenchyma

112
Q

What are the top 5 causes of glottic and subglottic stenosis?

A
  1. Iatrogenic causes such as prolonged ET intubation or laryngeal surgery
  2. External neck trauma
  3. Congenital stenosis
  4. Burns or caustic ingestions
  5. Infection
  6. Inflammation (s/a from GER or wegener granulomatosis)
113
Q

What are the types of stenosis?

A

Anterior
Posterior
Circumferential
Complete

114
Q

What is the most common if all laryngeal stenosis?

A

Chronic subglottic stenosis

115
Q

What is the pathogenesis of congenital stenosis?

A

Inadequate recanalization of the laryngeal lumen after completion of normal fusion at the end of the 3rd month of gestation.

116
Q

Where is the laryngeal defect in complete laryngeal atresia?

A

Glottis is closed at or above the vocal cords by a firm fibrous membrane

117
Q

Presentation of the most severe type of congenital laryngeal atresia?

A

Stillbirth

118
Q

Accounts for 5% of congenital anomalies of the larynx?

A

Congenital laryngeal webs

119
Q

Most common area for congenital laryngeal webs?

A

75% at glottic level, rest are supraglottic or subglottic

120
Q

Normal subglottic lumen diameter in full term neonate?

A

4.5 - 5.5 mm

121
Q

Normal subglottic lumen diameter in premature babies?

A

3.5 mm

122
Q

Considered narrowed subglottic diameter in a full-term neonate?

A

4 mm or less

123
Q

Top 3 most common congenital disorder of the larynx?

A
  1. Laryngomalacia
  2. Recurrent laryngeal nerve paralysis
  3. Subglottic stenosis
124
Q

2 types of congenital SGS?

A
  1. Membranous - fibrous soft tissue thickening of subglottic area caused by increased fibrous connective tissue or hyperplastic dilated mucous glands with no inflammatory reaction. Usually circumferential, narrowest area 2-3 mm below true VF
  2. Cartilaginous - mc type thickening or deformity of the cricoid cartilage that causes a shelflike plate of cartilage that partially fills the concave inner surface of the cricoid ring and extends posteriorly as a soft rigid sheet, leaving only a small posterior opening
125
Q

When do infants become symptomatic in SGS?

A

Within 3 mos of birth d/t increased activity and increased ventilation requirements

126
Q

______ of cases of acquired chronic SGS in infants and children occur secondary to ET intubation.

A

90%

127
Q

Incidence if stenosis after intubation?

A

Less than 1% to 8.3%

128
Q

Most commonly injured areas in ET intubation in children? In adults?

A

Subglottic region, posterior endolarynx

129
Q

In children, reasons the subglottic region is especially prone to injury from ET intubation?

A
  1. Cricoid cartilage is the only area in the upper airway that has a complete circular cartilaginous ring, which prevents the outward extension of traumatic edema
  2. The pseudostratified, ciliated, columnar respiratory epithelium lining this region is delicate and tends to deteriorate under the stress of an indwelling tube
  3. Subglottic mucosa is made up of loose areolar tissue that allows edema to develop easily and quickly
  4. Subglottic region is the narrowest portion of the pediatric airway
130
Q

Most cases of laryngeal trauma is completely healed after how many days?

A

30 days

131
Q

Safe intubation period in adults

A

7-10day period

132
Q

In children, et size should allow air leak at _______ if possible.

A

20cm water pressure

133
Q

2 safest materials for prolonged intubation?

A

Polymeric silicone and polyvinyl chloride

134
Q

What is anterior glottic stenosis?

A

Thin glottic web, which is a bridge of scar tissue covered by epithelium located between the vocal cords involving the anterior commissure.

135
Q

What is posterior glottic stenosis?

A

Due to prolonged ETT intubation. Scar is located in the interarytenoid space and posterior commissure. Posterior glottic scar frequently extends downward to subglottic region.

136
Q

What is interarytenoid adhesion?

A

The scar is between the vocal processes of the arytenoids with a small posterior, mucosally lined sinus tract in the posterior commissure area

137
Q

Anterior commissure benign lesions should be stages how many weeks apart for excision? (To prevent webbing)

A

2 weeks apart

138
Q

Symptoms of SGS usually occur how many weeks after the original insult?

A

2-4 weeks

139
Q

What is the grading for laryngeal stenosis by percentage of laryngeal lumen obstruction?

A

Grade I: 70%

Grade II: 70-90%

Grade III: >90%; identifiable lunen is present (no matter how narrow)

Grade IV: complete obstruction, no lumen

140
Q

How do corticosteroids tend to benefit in SGS?

A
  1. Decrease scar formation by their antiinflammatory action of delaying synthesis of collagen in early stages of wound healing and increasing collagen lysis in later phases
  2. Delay wound healing by delaying epithelial migration necessary to resurface the denuded area, thus increasing scar formation and predisposing to infection
141
Q

MOA of mitomycin C?

A

Antineoplastic antibiotic that acts as an alkylating agent by inhibiting DNA and protein synthesis

142
Q

2 main methods of repair for sgs?

A

Resection and expansion surgery.
Expansion surgery is a collection of techniques that aim to widen the glottic and subglottic lumen with success rates >90%

143
Q

Small anterior webs less than ______ mm wide produce minimal or no symptoms, and surgery is usually unneccessary.

A

2-3mm

144
Q

Gold standard in the assessment of the pediatric airway?

A

Bronchoscopy

145
Q

Classification of tracheomalacia?

A

Primary (intrinsic)

Secondary (compression)

146
Q

Preferred surgical treatment for long segment congenital tracheal stenosis with complete rings? For short stenosis?

A

Slide tracheoplasty

Segmental resection and reanastamosis

147
Q

Most common congenital anomaly of the esophagus?

A

Esophageal atresia with or without TEF

148
Q

Variation of Esophageal atresia most commonly encountered?

A

Esophageal atresia with distal TEF (85%)

149
Q

How many weeks gestation foregut develops a laryngotracheal groove which extends from the ventral aspect of the primordial pharynx caudal to the fourth branchial arches to produce a laryngotracheal bud?

A

4 weeks gestation

150
Q

What is the most commonly used classification system for tracheal agenesis (Floyd)?

A

Type I: proximal trachea is absent, and the airway connects to a distal TEF

Type II: (most common) carina arises from the lower esophagus

Type III: mainstem bronchi originate from 2 separate anastomoses with the esophagus.

151
Q

Patients with tracheal agenesis most commonly manifest with other features of VACTERL association which stands for?

A 
V - vertebral defects
A - anal atresia
C - cardiovascular defects
T - TEF
E - esophageal atresia
R - renal defects
L - limb defects
152
Q

Incidence of esophageal atresia?

A

1 in 3500

153
Q

Five types of Esophageal Atresia?

A
  1. EA with distal TEF (85%)
  2. Isolated EA without TEF (8%)
  3. H-type TEF (4%)
  4. EA with proximal TEF (3%)
  5. EA with proximal and distal TEF (1%)
154
Q

Up to 50% of patients with EA wil have other congenital anomalies, most commonly?

A

CV abnormalities

155
Q

How to diagnose EA?

A

Inability to pass 10F catheter beyond 10cm, excessive drooling, respiratory distress or cyanotic episodes

156
Q

Chest radiograph in EA with distal TEF?

A

Gastric bubble with air in proximal pouch

157
Q

Surgical treatment for EA?

A

Immediate gastrostomy followed by attempted primary anastamosis at 3 months

Foker technique - attempts to elongate the esophagus with external traction sutures prior to anastamosis

158
Q

Most common type of complete vascular ring? 2nd most common?

A
  1. Double aortic arch
  2. Right aortic arch with aberrant left subclavian artery and left ligamentum arteriosum

(These comprise 95% of complete rings)

159
Q

Pathogenesis of double aortic arch?

A

Distal right fourth branchial arch fails to involute

160
Q

Presentation of double aortic arch, with onset before 1 year of age.

A

Severe tracheomalacia

161
Q

In development, when the mid-left fourth arch involutes rather than the distal fourth arch (normal), this leads to an outpouching known as __________ from which arise an aberrant left subclavian artery and left ligamentum arteriosum?

A

Kommerell diverticulum

162
Q

Where does an abberant innominate artery arise from?

A

From an abnormally distal takeoff from the aortic arch and ascends over the anterior trachea about 1-2cm above the carina

163
Q

When does a left pulmonary artery sling develop?

A

When the left pulmonary artery arises from the right pulmonary artery and passes between the trachea and esophagus to cause compression of the right mainstem bronchus and distal trachea.

164
Q

Concurrent bronchomalacia is common and occurs in ______ cases of tracheomalacia.

A

30%

165
Q

How to diagnose tracheomalacia?

A

Bronchoscopy in a spontaneously ventilating patient. Decrease in luminal diameter greater than 50% at end expiration is diagnostic. Many patients with symptomatic TM show greater than 75% collapse

166
Q

Pathogenesis of primary tracheomalacia?

A

From intrinsic weakness of the trachea itself. (Higher incidence in premature infants)

167
Q

Normal trachea, cross sectional view displays what ratio of cartilaginous ring/posterior musculomembranous wall?

A

4.5 : 1

168
Q

Ratio of cartilaginous ring to posterior musculomembranous wall of trachea in primary TM? What is the manifestation on bronchoscopy?

A

2:1, narrow anteroposterior diameter and a widened posterior membranous wall on bronchoscopy

169
Q

What is the Cantrell and Guild structural classification for Congenital stenosis of the trachea?

A

Type 1: Generalized hypoplasia of the entire trachea

Type 2: Funnel stenosis: normal proximal trachea with distal narrowing to carina

Type 3: Segmental stenosis with up to three rings involves

170
Q

Most common associated anomaly with tracheal stenosis?

A

Pulmonary artery sling (in 50% of patients)

171
Q

What is the Anton-Pacheco Functional classification for congenital tracheal stenosis?

A

Mild - occasional or no symptoms

Moderate - Respiratory symptoms without respiratory compromise

Severe - Respiratory compromise
Subtype A : no associate malformations
Subtype B: associated malformations

172
Q

In children, what length of tracheal resection can be closed primarily?

A

2-3cm

173
Q

Dissection of strap muscles and mediastinal soft tissue can be done for what length of the trachea?

A

30%

174
Q

Intercartilaginous tracheal incisions afford what tracheal length?

Suprahyoid release?

Infrahyoid release?

Intrathoracic release?

A

1-2 cm

2-3 cm

2-2.5cm

3cm

175
Q

How to perform intrathoracic tracheal release?

A

Right intrapericardial hilar pulmonary release with division of the inferior pulmonary ligament

176
Q

What are the common airway foreign bodies?

A

Peanuts
Seeds
Vegetable matter

177
Q

What are the most common esophageal foreign bodies?

A

Coins and pins

178
Q

What are the most important factors in diagnosing an aerodigestive foreign body?

A

Reliable history and witnessed aspiration or ingestion

179
Q

Why is obstruction more common in the right main bronchus?

A

Wider lumen and more vertical path

180
Q

________ of esophageal foreign bodies that come to medical attention require endoscopic removal. ______ require open operative intervention.

A

10 - 20%

1%

181
Q

Why is obstruction of the right main bronchus more common?

A

Wider lumen and vertical path

182
Q

Three clinical phases of aspiration and ingestion of foreign bodies:

A
  1. Impaction
  2. Symtoms wane as foreign body settles into a stationary location and tracheoesophageal reflexes tire out
  3. Complications s/a obstruction, infection or perforation
183
Q

Mc presenting symptom of esophageal foreign body?

A

Vomiting (28%)

184
Q

Most reliable clinical findings for airway foreign bodies?

A

Cough
Decreased breath sounds
Wheezes

185
Q

Imaging tests of choice for aerodigetive foreign body?

A

Standard frontal and lateral radiographs

186
Q

Radiographic signs which indicate foreign body?

A
  • Unilateral emphysema
  • Hyperinflation
  • Localized atelectasis or infiltrates
  • Mediastinal or esophageal air trapping
187
Q

4 areas of physiologic narrowing of the esophagus?

A
  1. Upper esophageal sphincter
  2. Over aortic arch
  3. Over mainstem bronchus
  4. Lower esophageal sphincter
188
Q

Where do foreign bodies tend to lodge?

A

Just beyond cricopharyngeus muscle

189
Q

In young children, foreign bodies present for longer than _______ hours, sharp metallic or caustic foreign bodies should undergo urgent endoscopy.

A

24 hours

190
Q

Older asymptomatic child with midesophageal or distal may be observed for how long?

A

8 - 16 hours

191
Q

What percentage of asymptomatic children with recent (<24hours) ingestion without any underlying esophageal or tracheal abnormality wil have spontaneous passage of coin?

A

25-30%

192
Q

Mean intestinal transit time for an ingested foreign body?

A

3.8days

193
Q

Complication rate of aerodigestive endoscopy?

A

1 - 8%

194
Q

Most common complications of rigid bronchoscopy? (5)

A 
Failure to remove the foreign body
Laryngeal edema
Pneumothorax
Pneumomediastinum
Subcutaneous emphysema
195
Q

Why is organic matter associated with higher complication rate? (3)

A
  • Increased airway edema
  • Bronchial secretions
  • Tendency to develop a chemical bronchitis as a result of the proteins and oils contained in organic matter
196
Q

Effect of corrosive agents?

A

(Corrosive immediately dangerous to living tissue in contact with the agent)

Causes coagulation necrosis, a protein denaturation that leads to formation of a gel-like substance called the coagulum

197
Q

What is the mechanism of injury for caustic ingestion?

A

Strong alkali agents cause liquefaction necrosis, a process of early and rapid disintegration of mucosa with deep penetration into tissues. Forms a viscous liquid called saponification (formation if soap from fats and lye).

Blood vessel thrombosis comprises the tissue blood supply and further contributes to perforation

198
Q

What is the initial esophageal injury in caustic ingestion? (4)

A

Intense inflammatory reaction and edema
hemorrhagic congestion
eosinophilic necrosis
Bacterial invasion and saponification

199
Q

In caustic injury with partial thickness lesions, when does degeneration take place?

A

Within 24 hours in the epithelial layer followed by lymphocyte infiltration of the submucosa

200
Q

In full thickness corrosive injury, what esophageal layer is affected?

A

Muscular layer fibers

201
Q

By what day do fibroblasts and new blood vessels emerge in liquefactive necrosis?

When has necrosis finished?

When does granulation tissue predominate, and the contractile stage commences with stricture formation?

A

4th day

7th day

End of 2 weeks

202
Q

Most common symptom of caustic ingestion?

A

Vomiting

203
Q

3 layers of the esophagus?

A
  1. Mucosal outer layer
  2. Submucosal middle layer that contains fibrous connective tissue and mucous secreting glands
  3. Inner muscular layer
204
Q

Gold standard to stage extent of injury after caustic ingestion?

A

Endoscopy

205
Q

Best time to perform endoscopy?

A

Between 12 to 48 hours

206
Q

How to stage esophageal burns?

A

Grade 0: no injury

Grade I: mucosal edema and hyperemia

Grade IIa: superficial, noncircumferential, whitish membranes, shallow ulcers, hemorrhage, friable exudates

Grade IIb: deep, circumferential lesions with stricture formation

Grade IIIa: small, scattered areas of necrosis

Grade IIIb: extensive necrosis

Grade IV: perforation

207
Q

If more than 48 hours, what imaging can be done in lieu of endoscopy for caustic ingestion?

A

Chest and abdominal films

208
Q

Most common complication of caustic ingestion?

A

Stricture formation

209
Q

Esophageal carcinoma may arise in _______ of patients with strictures due to caustic ingestion.

A

1-4%

210
Q

Lithium batteries’ electrical current reacts with saliva to produce a hydrolysis with caustic injury that starts within how many hours?

A

2 hours

211
Q

What radiographic sign is critical in distinguishing button batteries from coins?

A

Double halo sign

212
Q

Characterized by immune mediated inflammation of the esophageal mucosa?

A

Eosinophilic esophagitis

213
Q

How to diagnose eosinophilic esophagitis?

A

Eosinophil density of at least 15 eosinophils/hpf in at least one microscopy field

Exclusion of GERD by absent response to PPI

214
Q

What are the four phases of swallowing?

A
  1. Oral preparatory
  2. Oral
  3. Pharyngeal
  4. Esophageal phases
215
Q

Anatomic sites of impairment which may account for characteristics of dysphagia?

A
  1. Nose and nasopharynx
  2. Oral cavity and oral pharynx
  3. Hypopharynx and larynx
  4. Trachea and esophagus
216
Q

Another term for modified barium swallow?

A

Videofluoroscopic swallow study

217
Q

Goals of VFSS?

A
  1. Determine whether anatomic or structural abnormalities are present
  2. Ascertain whether coordination if the structures and functions of the upper aerodigestive tract supports safe and sufficient bolus passage
  3. Identify strategies that enhance the safety and efficiency of feeding
218
Q

How to check for patency of the nasal airway?

A

Attempted passage of a 6-F feeding tube through the nares or by flexible fiberoptic endoscopy

Diplomate exam (7 decks)

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