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Pasha > Ch10. Peds Oto > Flashcards

Ch10. Peds Oto Flashcards

1
Q

Waldeyer’s Ring

A

Circle of lymphoid tissue including palatine/faucial tonsils, pharyngeal tonsils/adenoids, lingual tonsils, tubal tonsils of Gerlach (near fossa of Rosenmuller); lateral bands and posterior pharynegal wall complete the ring

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2
Q

Arterial supply to palatine tonsils

A
  1. Lingual artery (dorsal lingual br)
  2. Facial artery (ascending palatine and tonsillar arteries)
  3. Ascending pharyngeal artery
  4. Maxillary artery (greater palatine and descending palatine arteries
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3
Q

Venous drainage of tonsils

A

Lingual and pharyngeal veins (internal jugular vein)

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4
Q

Lymphatic drainage from tonsils

A

No afferent lymphatics, drainage into superior deep cervical and jugular digastric lymph nodes

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5
Q

Innervation to the tonsils

A
  1. Anterior pillar (CN X; palatoglossus)
  2. Posterior pillar (CNX; palatopharyngeus)
  3. Tonsillar fossa (CN IX, X; superior constrictors)
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6
Q

Histology/tonsillar zones (1st)

A
  1. Reticular epithelium: foreign material presented to lymphatic cells via 10-30 cryps/tonsil (blind tubules of squamous epithelium) -> antigen presenting cells (M-cells) -> lymphoid germinal center -> interdigitating dendritic cells and macrophages -> helper T cells -> memory B-cells (nasopharynegal or systemic migratino) and plasma cells (crypts)
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7
Q

Histology/tonsillar zones (2nd)

A
  1. Extrafollicular area: contains T-cells
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8
Q

Histology/tonsillar zones (3rd)

A
  1. Lymphoid follicle: composed of the mantzle zone (mature B-cells) and the germinal center (active B-cells)
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9
Q

What encapsulates the tonsils?

A

Tonsils encapsulated by special portions of pharyngobasilar fascia

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10
Q

Arterial supply to the adenoids

A

Ascending pharyngeal artery from external carotid, minor branches from maxillary artery (ascending pharyngeal branch), facial artery (ascending palatine artery), thyrocervical trunk (ascending cervical), artery of the pterygoid canal

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11
Q

Venous drainage from the adenoids

A

Pharyngeal veins -> facial and IJ

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12
Q

Innervation to the adenoids

A

CN IX, X

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13
Q

Histology of the adenoids

A

Ciliated pseudostratified columnar, stratified squamous, and transitional layers

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14
Q

Organisms of acute tonsillitis

A

Most commonly Group A beta-hemolytic streptococci, Moraxella, and H. influenzae; less common organisms include Bacteroides, staphylococci, E. coli, diphtheria, syphilis, Neisseria, and viruses (EBV, adenovirus, influenza A and B)

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15
Q

Phases of tonsillitis

A

Tonsillar erythema -> exudative tonsillitis -> follicular tonsillitis (yellow spots corresponding to lymphatic follicles) -> cryptic tonsillitis (chronic infection)

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16
Q

Chronic adenoiditis pathophyz and SSx

A

Typically a polymicrobial infection; may be related to reflux, especially in children (difficult to distinguish from sinusitis)
SSx: persistent nasal discharge, malodorous breath, nasal obstruction (snoring), association with recurrent otitis media and sinusitis

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17
Q

How to determine hyponasal speech (i.e. adenoid hyperplasia)?

A

Pinch nose does not change speech, “M” words

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18
Q

What is adenoid facies?

A

Open mouthed, dark circles under eyes, flattened midface, high arched palate

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19
Q

What to suspect if unilateral tonsillar hyperplasia?

A

Consider neoplasm (lymphoma, leukemia, SCC) or unusual infections (M. tuberculosis, atypical mycobacteria, actinomycosis, fungal)

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20
Q

What to do in acute respiratory distress from obstructive tonsillar and adenoid hypertrophy?

A

Use nasal trumpet (rarely requires intubation) with a short course of corticosteroids, prolonged course of Abx (3-6 weeks) or nasal corticosteroid sprays for adenoid hyperplasia; tonsillectomy and adenoidectomy for definitive therapy

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21
Q

PTA pathophyz( two)

A
  1. Spread of infection outside tonsillar capsule into the peritonsillar space
  2. Infection in a peritonsillar minor salivary gland (Weber gland), controversial
    Typically begins at superior pole
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22
Q

Uvular deviation in PTA

A

To the contralateral side

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23
Q

Infections mononucleosis pathophyz

A

EBV (Ebstein-Barr virus) selectively infects B-lymphocytes (90%); CMV and other viruses less commonly involved (10%)

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24
Q

Dx test for Mono

A

Heterophile antibodies in serum (Monospot test, Paul Bunnell test; rapid kits 85% sensitive, ~100% specific) will be 40% negative in first 2-3 weeks
Presence of 80-90% mononuclear and 10% atypical lymphocyets on smear
IgM firs tmonth only; IgG appears at 1 week, present for life

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25
Q

Abx in Mono

A

Antimicrobials for secondary infections (amp/amox may cause a severe rash from hypersensitivity)

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26
Q

Sleep physiology of newborn

A

<2 months
Preterm: sleep staged differently; quiet, active, and intermediate sleep; quiet is similar to NREM, active is similar to REM (~50%), intermediate is mix
Term: sleep/wake differentiation occurs by 37 weeks GA

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27
Q

Sleep physiology of infant

A

2mo-1yr

Percentage of REM sleep declines

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28
Q

Sleep physiology of toddler

A

1-3 yrs
1 yr: 30% REM, may nap 1-2 hours/day, normal sleep time 13-15 hours
2 yr: 25% REM similar to adults, separation anxiety and night awakenings

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29
Q

Sleep physiology of school age/prepubescent

A

5 yr: 20% REM, naps not required, adult-like sleep cycles (90-110 minutes)
6-12 yrs: slow wave sleep is maximal, then abruptly drops off in puberty and declines throughout adulthood; circadian phase preferences develop (morning versus evening); parasomnias may develop

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30
Q

Sleep physiology of adolescent

A

should get 9 hrs of sleep

at risk for behavior-induced insufficient sleep syndrome

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31
Q

Peds sleep-disordered breathing

A

Defined as: abnormal respiratory pattern during sleep that includes snoring, mouth breathing, and pauses in breathing

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32
Q

Spectrum of SDB

A

Snoring (10%)
Upper airway resistance syndrome
Obstructive hypoventilation
Obstructive sleep apnea (OSA: 1-3%)

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33
Q

Pathophyz of SDB

A

Upper airway osbruction from adenotonsillar hyperplasia MC
Obesity (25-40% have SDB
Carniofacial anomalities/syndromes
Prematurity
Daycare exposure and freq URI, smoking exposure
Ethnicity (Af-am MC)
Neuromuscular disorders

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34
Q

Indications for PSG in SDB (AAO-HNS CPG 2011)

A
  1. Prior to tonsillectomy in presence of obesity, Down syndrome, craniofacial anomalies, neuromuscular disorders, sickle cell disease, mucopolysacchridoses
  2. Discordance between tonsillar size and SDB symptoms
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35
Q

Peds OSA complications

A

DD, FTT (increased energy expenditure, feeding impairment, reflux from high negative intrathoracic pressures), cardiorespiratory complications (cor pulmonale, pectus excavatum), behavioral disorders

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36
Q

Peds PSG sleep scoring: apneic events

A

Drop in airflor >=90% (oronasal thermal sensor) that lasts the duration of 2 baseline breaths (does NOT req 10 seconds)

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37
Q

Peds PSG sleep scoring: hypopneic events

A

Nasal air pressure decreases by >= 30% lasting the duration of 2 breaths and must be associated with a >=3% oxygen desaturation or an arousal/awakening

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38
Q

Peds PSG sleep scoring: respiratory effort related arousals/RERAs

A

nasal air pressure flattens and decreases in amplitude but NOT >= 30% and is associated with snoring, noisy breathing, incerased work of breathing or elevation of end-tidal or transcutaneous PCO2

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39
Q

Peds PSG sleep scoring: AHI

A

Apnea-hypopnea index, number of obstructive apneas and hypopneas per hour of sleep

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40
Q

OSA scoring scale (AAO-HNS CPG 2012)

A
  1. Normal AHI <= 1, O2 nadir >92%
  2. Mild OSA: AHI >1, <= 5
  3. Mod OSA: AHI >5, <= 10
  4. Severe OSA: AHI >10, O2 nadir <80%
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41
Q

Hypoventilation syndrome

A

if arterial (or end-tidal) CO2 >50 mm Hg for >25% of total sleep time

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42
Q

Central sleep apnea

A

similar to adults but event must last >= 20 seconds or 2 missed breaths with an arousal/awakening or with a >=3% desaturation
Consider medical causes, Arnold Chiari malformation, metabolic disorders, cardiac disease, medications (opioids), high altitude

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43
Q

Primary sleep apnea of infancy

A

Central apnea of >=20 seconds associated with immaturity of brainstem respiratory control centers
Lead to bradycardia and hypoxemia, may require resuscitation or stimulation
More common in preemies

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44
Q

Periodic breathing

A

series of 3 episodes of central apneas lasting >3 seconds each occuring within 20 seconds
Frequent in Arnold-Chiari patients

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45
Q

Congenital central hypoventilation syndrome (Ondine’s Curse)

A

PHOX2b gene mutation causing a failure of autonomic control of breathing at night
Rx: tracheotomy and long-term ventilation during sleeps/naps

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46
Q

Sudden infant death syndrome

A

Abrupt, unanticipated death of unknown etiology
RFs: male, preemie, prone position sleep, multiple births, maternal young age (teen), family hx
Prevent by supine position sleep (“back to sleep”), firm mattress, no bed sharing, removal of surrounding soft objects

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47
Q

Behavior insomnia of childhood: sleep-onset type

A

caused by reliance on an inappropriate sleep association and inability fo “self soothe” (e.g., rocking, bottle, parents’ bed)
Rx: CBT, extinction (“crying it out”), gradually reduced parent intervention, daytime naps, discontinued feeding after 6 months, consider preemtive scheduled awakenings (!5 minutes before anticipated awakening)

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48
Q

Behavior insomnia of childhood: limit-setting type

A

characterized by parents’ inability to establish appropriate sleep behaviors, “child stalling” or refusals
Rx: CBT, consistent bedtime, parent education, may provide a transitional object (e.g., stuffed animal, blanket)

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49
Q

Patient care recommendations from AAO-HNS CPG 2011

A
  1. Preop: avoid anxiolytics or sedatives; if nec, then monitor for hypoventilation and hypoxemia
  2. Intraop: intraop Decadron reduces postop nausea/vomiting; SDB children are at increased risk of airway collapse and delayed emergency; avoid or reduce intraop opioids for SDB children; local anesthesia injection should NOT be used
  3. Postop: SDB children require more intensive nursing care and monitoring; strong recc against periop Abx (not shown to reduce postop hemorrhage, pain, or return to normal function significantly)
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50
Q

Pain control after tonsillectomy

A

Tylenol and ibuprofen
Codeine not recc; postop opiates must be used with caution (abnormal metabolism related to CYP2D6, causing overproduction of metabolites)
Ketorolac contraindicated due to increased bleeding risk

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51
Q

Monitored overnight stay after tonsillectomy

A

Considered in <3 years old, syndromic, comorbidities, obesity (>99th percentile BMI), live >1 hour from hospital, unreliable parents, bleeding disorder, or severe OSA (AHI >=10, O2 nadir <80%)
REM rebound may occur in severe OSA patients after 18hrs, which may cause hypoventilation and hypoxemia

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52
Q

ICU admission after tonsillectomy

A

Severe OSA, comorbidities that cannot be managed on a ward, significant airway obstruction and O2 desat in recovery room unresponsive to repositioning and O2

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53
Q

Tonsillectomy indications

A
  1. Tonsillar hyperplasia resulting in SDB or OSA associated with cor pulmonale
  2. Suspected malignancy
  3. Tonsillitis resulting in febrile convulsions (may require Quinsy tonsillectomy)
  4. Persistent or recurrent tonsillar hemorrhage
  5. FTT (not attiributable to other causes)
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54
Q

What is Paradise criteria?

A 
Relative indication for tonsillectomy
7 infections in 1 year
5 infections/yr x2
3 infections/yr x3
(infx defined as sore throat with 1+ more of fever >38.3, cervical adenopathy, tonsillar exudate, or pos strep test)
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55
Q

Most common complications after T&A?

A

Most common serious complication is bleeding (0.5-5%)

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56
Q

Types of bleeding T&A complications

A

Three.

  1. Intraoperative
  2. Immediate post-op
  3. Delayed post-op
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57
Q

Describe intraoperative T&A bleeding complications.

A

Arterial injury such as aberrant carotid artery, retrained tonsillar tissue, tears in posterior pharyngeal wall

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58
Q

Describe immediate postoperative bleeding after T&A

A

Bleeding <24 hrs post-op. 0.2-2.2%.

Similar to intraoperative, may be due to inadequate hemostasis during surgery typically from vessel spasm

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59
Q

Describe delayed post-op bleeding after T&A

A

> 24hrs post-op. 0.1-3%.

~5-10 days post-op, due to eschar sloughing

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60
Q

Describe post-op edema after T&A

A

Due to sudden relief of airway obstruction from long-standing adenotonsillar hyperplasia resulting in a sudden drop in intrathoracic pressure, increased pulmonary blood volume, and increased hydrostatic pressure
May occur immediately or after a few hours
Rx: PEEP, mild diuresis

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61
Q

Describe VPI after T&A

A

Results from an incompetent velopharyngeal inlet; increased risk with submucosal cleft palate, history of nasal regurgitation, or preoperative hypernasality
Rx: speech therapy (typically resolves); if persistent pharyngeal flap or palatal lengthening and consider testing for 22q11

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62
Q

Describe Grisel syndrome

A

Atlantoaxial (C1-C2) subluxation resulting in spread of inflammation from the OP to the cervical ligaments resulting in laxity and spinal cord compression; rare, increased risk with Down syndrome
Rx: orthopedic consult, may need Abx, cervical collar

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63
Q

Ideal age for septoplasty?

A

After puberty (~15-16 years old)

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64
Q

Describe mandibular distraction osteogenesis

A

Progressive elongation of native mandible and soft tissue envelope by performing bilateral sagittal osteotomies and placement of internal and external distraction devices

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65
Q

indications for MDO

A

Micrognathia/retrognathia, airway obstruction, feeding difficulties, tracheostomy decannulation, severe obstructive sleep apnea, hemifacial microsomia
Commonly performed for Pierre-Robin Sequence and Treacher Collins, Nager, velocardiaofacial and Pfeiffer syndromes

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66
Q

Phases of MDO?

A

Four.

  1. Lacenty
  2. Active distraction
  3. Consolidation
  4. Hardware removal
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67
Q

Latency phase of MDO?

A

First one of four.
1-5 days; shorter in toddlers/young children, wait 5-7 days in adults; allows hematoma formation and platelet-derived growth factor production; if too short may lead to fibrous union and if too long may lead to callus

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68
Q

Active distraction phase of MDO?

A

1-2 mm/day until supraglottic obstruction relieved

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69
Q

Consolidation phase of MDO?

A

4-12 weeks

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70
Q

Complication of MDO

A

Infection, scarring, nerve injury (marg, inferior alveolar, facial nerve), dental injury (tooth bud injury with tooth loss, dentigerous cysts), malocclusion (anterior open bite), poor healing (malunion, nonunion, relapse), device failure, TMJ ankylosis

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71
Q

Most common H&N neoplasm in children

A

Infantile hemangioma

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72
Q

Origin of infantile hemangioma

A

Endothelial origin

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73
Q

Presentation of infantile hemangioma

A

Superficial type presents at birth or within 2 weeks as a white spot (Herald Path) or a small red spot; deep type usually discovered a few weeks after birth

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74
Q

Epidemiology of infantile hemangioma

A 
MC female (3:1 ratio)
10% population incidence
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75
Q

Pathophysiology of infantile hemangioma

A

Unknown, possibly from disrupted placental cells or stem cells

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76
Q

Histopathology of infantile hemangioma

A

IHC markers GLUT1 and LeY (Lewis Y antigen)

Biological markers: beta-fibroblast growth factor, urokinase

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77
Q

Stages of infantile hemangioma

A
  1. Proliferative <= 12 months old, endothelial cell hyperplasia, elevated mast cells, multilaminar basement membrane
  2. Involuting 50% regress by 5 years old, 70% by 7 years; fibrosis, decreased cellularity
  3. Involuted: soft mass of excess skin and fibrofatty tissue, scarring, telangiectasias, atrophy
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78
Q

Types of infantile hemangioma

A
  1. Superficial/cutaneous (strawberry or capillary hemangioma): bright strawberry-red color progresses to wind color then grey
  2. Deep (cavernous hemangioma): covered by skin, appears blue
  3. Compound: mixed
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79
Q

Define PHACES Syndrome

A

Posterior cranial fossa anomalies (req MRI)
Hemangioma (facial segmental)
Arterial/carotid anomalies
Cardiac anomaly/Coarctation of the aorta (req cardiac echo)
Eye anomaly
Sternal pit
MC females (90%); consider if large segmental hemangioma

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80
Q

Maffucci Syndrome

A

Multiple deep hemangiomas +/- visceral vascular lesions
Dyschondroplasia
Chondrosarcoma in 25%

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81
Q

Complications of infantile hemangioma

A

In 20%
Cosmetic deformity, amblyopia (eye involvement), ulceration (10%), infection, bleeding (rare, reassure that it will not “burst”), airway compromise (laryngeal), thrombocytopenia, and high output cardiac failure (rare)

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82
Q

Dx for Subglottic Hemangioma

A

Endoscopy (avoid biopy), CT and MRI may confirm diagnosis

PA and lateral neck x-rays may show unilateral or posterior subglottic lesion

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83
Q

Describe cutaneous infantile hemangioma

A

MAy present anywhere in H&N (concerning in eyelid and orbit)
Common in parotid and oral cavity (lip), 1% of children with a cutaneous lesion will have a subglottic hemangioma

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84
Q

Describe laryngeal infantile hemangioma

A

Sessile lesions, present with inspiratory or biphasic stridor within the first few months of life that is worse with crying (engorgement), dysphonia, dysphagia (rare)
50% of children with a subglottic hemangioma will have a cutaneous lesion

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85
Q

Describe nasal infantile hemangioma

A

MC in Little’s area (Kisselbach’s plexus) or inferior turbinate

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86
Q

Describe ear/periauricular infantile hemangioma

A

May deform the ear or ear canal (CHL)

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87
Q

Describe parotid infantile hemangioma

A

50% of parotid hemangiomas associated with cutaneous hemangiomas

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88
Q

When should one order ultrasound in infantile hemangioma?

A

If >3 hemangiomas, consider abdominal ultrasound for occlult lesions (eg liver)

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89
Q

Define complications from infantile hemangioma

A 
VASCO
impaired Vision or hearing
imparied Swallowing
important Cosmetic effect or with ulceration
high Output cardiac failure
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90
Q

Rx infantile hemangiomas without complications

A

Observation, propranolo, oral steroids, surgical excision (cold or pulsed dye laser)

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91
Q

Rx infantile hemangiomas with complications

A

Propranolol is standard of care for hemangiomas in the proliferative stage, consider trial of oral steroids if >12 months old, consider vincristine for severe cases

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92
Q

Propranolol considerations in infantile hemangiomas

A

Baseline vital signs, recent normal cardiovascular and pulmonary exams (ECG or glucose screening no longer req w normal exam)
Usually responds within 2-12 weeks; continue until 1 year old then taper
Contraindications include cardiogenic shock, sinus bradycardia, hypotension, greater than first-degree heart block, heart failure, bronchial asthma, and drug hypersensitivity (higher stroke risk in PHACES)

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93
Q

Two types of congenital hemangioma

A

Congenital hemangioma is present at birth

  1. RICH: rapidly involuting, involutes by 6-14 months; typically GLUT-1 neg
  2. NICH: non-involuting, does not involute; GLUT-1 negative. Rx: surgery; consider preoperative angiography with embolization for large lesions.
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94
Q

Define TA and KHE

A

Tufted angioma (TA) and kaposiform hemangioendothelioma (KHE) are a spectrum of vascular tumors of arteries and veins that are GLUT-1 negative

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95
Q

Describe TA to KHE

A

Congenital or acquired
>50% present <1 year old
Variable growth and regerssion paterns

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96
Q

Describe KHE growth pattern

A

Aggressive permeating muscle, soft tissue and bone

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97
Q

Describe TA/KHE histopathology

A

Hypercellular tufts of capillaries in the reticular dermis
May be associated with dilated lymphatic vessels
Deeper spindle cells indicate KHE
Positive for D2-40 (lymphatic marker)

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98
Q

Describe SSx of TA/KHE

A

Macules/patches (mottled red), plaques (red-purple, indurated), annular patterns of presentation; tenderness; hyperhidrosis, hypertrichosis (hard on palpation)

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99
Q

Describe visceral involvement of TA/KHE

A

Visceral involvement almost always associated with platelet trapping

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100
Q

How to diagnose congenital hemangioma?

A

CBC, DIC (diffuse intravascular coagulation) panel, MRI, biopsy if needed (may need in >1 location)

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101
Q

Rx for congenital hemangioma

A

Observation, cryotherapy, pulsed dye laser, surgical excision

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102
Q

Define Kasabach-Merritt Phenomenon

A

Sequestration of platelets and severe thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy in KHE or TA (not infantile hemangioma)
Suspect with rapidly enlarging lesion
Can be life-threatening

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103
Q

Rx Kasabach-Merritt Phenomenon

A

Drug combinations/chemotherapy (vincristine) or surgery

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104
Q

Define vascular malformations

A

Vascular channel malformations secondary to a defect in morphogenesis
Characterized as high flow (arteriovenous) or low flow (lymphatic, capillary, venous) malformations

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105
Q

How are vascular malformations different from hemangiomas?

A

VM are present at birth (although may manifest later secondary to hormonal changes, severe infections near vessels or trauma)
Grows with child (endothelium hypertrophies) and therefore does not regress
Sudden increase in size is concerning

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106
Q

Histopathology of vascular malformations

A

Mature endothelium with normal mitosis (versus hemangioma, which has increased mitosis in the proliferative phase

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107
Q

Associated symptoms of vascular malformations

A

Sturge-Weber syndrome
Klippel-Trenaunay syndrome (KTS; combination of capillary, venous, and lymphatic types of VM)
Parkes-Weber syndrome (arteriovenous and capillary malformation in association with skeletal/soft tissue hypertrophy)
Blue rubber bleb (venous malformation with associated GI lesions)

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108
Q

Sturge-Weber syndrome

A

(SWS; unilateral port-wine stain in CN V1 distribution with extension to the leptomeninges)

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109
Q

Klippel-Trenaunay syndrome

A

(KTS; combination of capillary, venous, and lymphatic types of VM)

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110
Q

Parkes-Weber syndrome

A

(arteriovenous and capillary malformation in association with skeletal/soft tissue hypertrophy)

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111
Q

Blue rubber bleb

A

(venous malformation with associated GI lesions)

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112
Q

Types of low flow vascular malformations

A
  1. Lymphatic malformation
  2. Capillary malformation
  3. Venous malformation
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113
Q

Epidemiology of lymphatic malformations

A

90% present <3 years old (65% present at birth)
May persist in adulthood
Associated with venous malformations (lymphatics and venous system develop concurrently)

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114
Q

Histopathology of lymphatic malformation

A

Abnormal development or obstruction of primitive jugular lymphatics that undergo irregular growth with lymphoendothelial hyperplasia
Increase in mast cells during proliferative phase, fewer mast cells during the involutional stage (D2-40 stain)

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115
Q

Classification of lymphatic malformation

A

Macrocystic (>=1 cysts, >= 2mL)
Microcystic (<2 mL)
Mixed (formerly called cystic hygroma and lymphangioma)

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116
Q

What are cystic hygroma and lymphangioma now?

A

Mixed lymphatic malformation

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117
Q

Staging of lymphatic malformation

A 
Modified de Serres
I: unilateral infrahyoid
II: unilateral suprahyoid
III: unilateral infrahyoid and suprahyoid
IV: bilateral infrahyoid and suprahyoid
V: bilateral infrahyoid and suprahyoid
VI: bilateral infrahyoid and suprahyoid
VII: retropharyngeal
M: mediastinal extension (I-III typically macrocystic and IV-VI typically microcystic)
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118
Q

SSx of lymphatic malformation

A

Soft painless compressible mass (lymphatic dilation) with skin discoloration (macrocystic); soft noncompressible masses with mucosal or skin vesicles (microcystic); both types may cause dysphagia, dyspnea; may remain dormant; may become painful with acute infection

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119
Q

Dx lymphatic malformation

A

Physical exam, MRI

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120
Q

Complications from lymphatic malformation

A

Respiratory distress from respiratory tract compression, infection (common, presents as a rapid enlargement of the malformation), disfigurement, spontaneous hemorrhage into macrocysts causing rapid enlargement

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121
Q

Rx lymphatic malformation

A

Sclerotherapy (doxycycline, bleomycin), sirolimus (rapamycin), early conservative excision when symptomatic (spare vital structures), low rate of recurrence if compeltely removed (only 50% if gross tumor remains); if detected prenatally and airway concerns, may require EXIT procedure

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122
Q

Define capillary malformation

A

Also called port-wine stain, stork bite, salmon patch (nape of the neck) or angel kiss (forehead)

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123
Q

Classification of capillary malformation

A

Medial (salmon patch, usually lightens and disappears with time)
Lateral (port-wine stain, always persists, usually follows CN V on face and darkens with time; involvement of lateral thigh and knee indicates Klippel-Trenaunay syndrome

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124
Q

SSx of capillary malformation

A

Bright red, scarlet at birth fades to pink in infants but then gradually enlarges and deepens to dark purple by adulthood
Medial type is lighter at birth

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125
Q

Rx of capillary malformation

A

Pulsed dye laser

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126
Q

Define venous malformation

A

Ectatic venous channel network which has a tendency to grow slowly in childhood, then expand rapidly with hormonal changes or trauma
Often involves the aerodigestive tract

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127
Q

SSx of venous malformation

A

Compressible mass, skin discoloration (none to dark blue/purple); airway obstruction, dysphagia,; symptoms often get worse with recumbent position or Valsalva

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128
Q

Dx of venous malformation

A

Physical exam, Doppler ultrasound, MRI

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129
Q

Rx of venous malformation

A

Surgery, laser, sclerotherapy (sodium tetradecyl sulfate, ethanol), anticoagulatns for symptomatic thrombosis

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130
Q

Types of high flow vascular malformations

A

Only arteriovenous malformation (AVM)

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131
Q

Define arteriovenous malformation

A

Shunting between the arterial systems via anomalous capillary beds

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132
Q

Growth of AVM

A

typically small and stable in childhood, then rapid growth in 2nd-3rd decade of life with puberty and/or trauma

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133
Q

AVM Staging

A

Schobinger staging
Stage I: quiescent
Stage II: expansion (bruit, thrill, warm throbbing)
Stage III: destruction (ulcers, bleeding, bony changes)
Stage IV: systemic (congestive heart failure, left ventricular hypertrophy)

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134
Q

SSx of AVM

A

Warm, pulsatile intermittently growing lesion with skin discoloration; bruit

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135
Q

Dx of AVM

A

Physical exam, pulsed Doppler, CTA, MRA and sometimes still digital angiography

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136
Q

Complications from AVM

A

Local tissue destruction and hemorrhage

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137
Q

Rx for AVM

A

Embolization; some require surgical excision

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138
Q

When are newborns preferential nasal breathers?

A

For 6-20 weeks (variable)

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139
Q

When should you suspect nasal obstruction?

A

Newborns with tachypnea, cyclical cyanosis (worse with feeding, improve with crying) FTT, rhinorrhea, unable to pass 6 French flexible suction catheter

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140
Q

Dx congenital nasal disorders and neonatal nasal obstruction

A

Assessment for dysmorphisms (telecanthus, broad nasal bridge, nasal pits), ocular discharge, periocular infection/edema, nasal endoscopy, oral exam (palate arching or clefting), CT or MRI if tumor suspicion

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141
Q

DDx of congenital nasal disorders and neonatal nasal obstruction

A

Rhinitis of the newborn, viral rhinitis, dacryocystocele, prifirom aperture stenosis, midnasal stenosis, choanal atresia, tumors (encephalocele, glioma, dermoid, teratoma, hemangioma), septal deviation (birth trauma, rare)

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142
Q

Rx for congenital nasal disorders and neonatal nasal obstruction

A

Address underlying cause, for bilateral obstruction or airway distress consider an oral cannula (McGovern nipple, oral airway) prior to intubation, tracheotomy reserved for severe cases

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143
Q

What is a McGovern nipple?

A

Large nipple with end cut off

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144
Q

Define idiopathic rhinitis of the newborn

A

Considered after negative work-up for nasal obstruction and other causes of rhinitis

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145
Q

Pathophysiology of idiopathic rhinitis of the newborn

A

Possibly secondary to maternal estrogen, infectious (congenital syphilis “snuffles”, chlamydia), early allergic rhinitis (high prevalence of familial atopy), ciliary dyskinesia, hypothyroidism

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146
Q

SSx of idiopathic rhinitis of the newborn

A

Abundant rhinorrhea (mucoid), nasal mucosal edema, stertor, tachypnea, poor feeding

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147
Q

Rx for idiopathic rhinitis of the newborn

A

Frequent suctioning, nasal saline sprays, nasal steroid drops, avoid stenting if possible

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148
Q

Peds allergic rhinitis associated SSx

A

decreased energy and stamina, sleep deprivation, limitaitons in organized sports and outdoor activities, poor school performance

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149
Q

Risk factors for peds allergic rhinitis

A

urban living, obesity, no breast feeding, environmental tobacco smoke

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150
Q

Complications of peds allergic rhinitis

A

Asthma exacerbation (asthma in 48% of AR patients, but rhinitis in 80% of asthma patients, risk of asthma related to severity and duration of rhinitis), sinusitis, otitis media, sleep disorders, craniofacial abnormalities (upturned nose or “allergic salute,” elongated “adenoid” facies), decreased cognitive functioning

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151
Q

When to consider immunotherapy?

A

Sublingual and intradermal immunotherapy may be considered >4-5 years old, may be protective against new sensitivities and development of asthma

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152
Q

Pathophysiology of choanal atresia

A

Persistence of the bucconasal membrane or abnormal migratio of neural crest cells into the nasal vault resulting in a complete bony (30%), mixed bony-membraneous (70%), or membranous (rare) defect of the posterior nasal cavity
Bony components are from the pterygoid plate and vomer

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153
Q

Epidemiology of choanal atresia

A

MC females; unilat (65%; R>L)

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154
Q

SSx of choanal atresia

A

Unilateral presents with rhinorrhea, nasal obstruction
Bilateral presents at birth with cycles of apnea and cyanosis followed by crying due to obligate nasal respiration in neonates

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155
Q

Dx choanal atresia

A

Mirror to detect condensation, attempt transnasal passage of 6 French catheter, attempt nose blowing with an occluded nostril, nasal endoscopy, CT

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156
Q

Associated syndromes with choanal atresia

A

CHARGE syndrome (MC concurrent syndrome in bilateral atresia, 50%), Apert, Treacher Collins, Crouzon, trisomy 21, 22q11 deletion

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157
Q

Rx for choanal atresia

A

Surgical repair via transnasal (usually endoscopic), transantral (creation of large cavity for recurrent cases), transseptal, or transpalatal (classic operation, may disrupt orthodontic growth, less common today) appraoch
Post-op stenting less common with endoscopic repair; unilateral atresia may be repaired electively
Bilateral atresia must be addressed during first weeks of life, early meausre includes establishing an oral airway (eg, McGoevrn nipple) intubation not usualyl required

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158
Q

DDx unilateral peds nasal mass

A 
Vascular (JNA, hemangioma, AVM)
Infectious/inflammatory (polyp, rhinolith)
Neoplastic/mass (encephalocele, glioma, neurofibroma)
Drug-related
Idiopathic
Congenital (nasolacrimal duct cyst)
Autoimmune/allergic
Truamatic (foreign body)
Endocrine
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159
Q

Fonticulous frontalis

A

Embryologic space that normally fuses during teh development of the frontal bones

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160
Q

Prenasal space

A

Embryologic spaces between the nasal bone and nasal cartilage

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161
Q

Foramen cecum

A

Region between ethmoid and frontal bones, connects with prenasal space

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162
Q

Pathophysiology of neurogenic tumors

A

Dura projects through the foramen cecum, the fonticulus frontalis (intranasally), or the prenasal space into skin (extranasally) with failure of anterior neuropore closure

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163
Q

Dx neurogenic tumors

A

MRI/CT to evalute intracranial extention

Do not biopsy

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164
Q

Pathophysiology of encephalocele

A

failured closure of neuropore or failed migration of neural crest cells results in ependymal-lined meninges herniation through the base of skull
Communicates with subarachnoid space (CSF filled)

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165
Q

Types of encephalocele by layers

A

MC lumbar-sacral region

  1. Meningocele: meninges only
  2. Meningoencephalocele: meninges and brain elements
  3. Meningoencephalocystocele: meninges, brain, and a part of the ventricular system
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166
Q

Types of encephalocele by location

A
  1. Occipital: most common (75%)
  2. Sincipital (frontoethmoidal): defect between frontal and ethmoid bones at the foramen cecum; nasofrontal (glabellar lesion), nasoethmoidal (lateral nose lesion), and nasoorbital (medial orbital wall lesion) subtypes
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167
Q

SSx of encephalocele

A

Bluish, soft, pulsatile, compressible mass that changes with straining and crying, transilluminates
Intranasal encephaloceles often confused with nasal polyps

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168
Q

Dx of encephalocele

A

CT/MRI reveals bony defect

Furstenburg test

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169
Q

What is Furstenburg test?

A

Compression of IJ cuases increases in size of the mass due to increased CSF pressure

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170
Q

Complications of encephalocele

A

meningitis, nasal obstruction, cosmetic deformity, hydrocephalus

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171
Q

Rx for encephalocele

A

surgical excision similar to glioma, must also close the dural defect to prevent CSF leak and brain herniation (neurosurgical consultation)

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172
Q

Pathophysiology of nasal glioma

A

Sequestered glial tissue or “pinched off encephalocele” results in unencapsulated collection of heterotopic glial cells
15% connect to dura by a fibrous stalk

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173
Q

Location of nasal glioma

A

Extranasal (60%) or intranasal (30%), typically not midline

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174
Q

SSx of nasal glioma

A

Firm, nonpulsatile mass, skin-covered, does nto change in size with straining, noncompressible, does not transilluminate, may look like intranasal polyp, broad nasal dorsum

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175
Q

Dx of nasal glioma

A

CT and/or MRI to evaluate for intracranial extension (15%), neg Furstenburg test

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176
Q

Complications of nasal glioma

A

Meningitis, nasal obstruction, cosmetic deformity

177
Q

Rx for nasal glioma

A

Surgical excision (intranasal appraoch for small tumors, extranasal appraoch for larger tumors), may require craniotomy for intracranial involvement (neurosurgical consultation)

178
Q

What is the most common midline nasal mass?

A

Nasal dermoid

179
Q

Pathophysiology of nasal dermoid

A

defective obliteration of dural tissue in prenasal space or fonticulus frontalis forms a dermal cyst

180
Q

Which germ layers for nasal dermoid?

A

May contain both mesodermal and ectodermal components including adnexal tissue (hair follicles, sweat glands, sebaceous glands)

181
Q

Location of nasal dermoid

A

MC at nasal dorsum but may occur anywhere from glabella to nasal tip (extranasal, intranasa, or intracranial)

182
Q

SSx of nasal dermoid

A

Presents at birth; forms a fistulous tract, pit, or cyst
Firm, noncompressibel, does not transilluminate
Tuft of hair may protrude from pit

183
Q

Dx of nasal dermoid

A

CT and/or MRI to evaluate for intracranial extension (@5%), negative Furstenburg test

184
Q

Complications of nasal dermoid

A

Meningitis, CSF leak, repeated local infection, cosmetic deformity

185
Q

Rx for nasal dermoid

A

Meticulous excision, must excise complete tract (usually subcutaneous although may dive deep into nasal bone and intracranially)

186
Q

Pathophysiology of Rathke’s cleft cyst

A

Persistent craniopharyngeal canal from failure of the obliteration of Rathke’s pouch (a diverticulum of ectoderm that invaginates to form the anterior pituitary and pars intermedius)

187
Q

What is the Rathke’s pouch?

A

A diverticulum of ectoderm that invaginates to form the anterior pituitary and pars intermedius

188
Q

Location of Rathke’s pouch

A

Nasopharynx

189
Q

SSx of Rathke’s pouch?

A

Typically asymptomatic, smooth mass in nasopharynx, may enlarge and impinge on the pituitary

190
Q

Dx of Rathke’s pouch

A

CT or MRI, biopsy

191
Q

Rx for Rathke’s pouch

A

Endoscopic removal or marsupialization if symptomatic, antibiotics if infected

192
Q

What is another name for nasolacrimal duct cyst?

A

Dacryocystocele

193
Q

Pathophysiology of dacryocystocele

A

Failure of opening of the distal nasolacrimal duct (valve of Hasner) with cyst formation from accumulation of secretions

194
Q

Location of dacryocystocele

A

Nasolacrimal duct (anteriorly in the inferior meatus)

195
Q

SSx of dacryocystocele

A

Usually asymptomatic, epiphora, nasal obstruction, may cause respiratory distress and difficulty feeding in infants with large obstructive cysts (obligate nasal breathing)

196
Q

When do dacryocystocele resolve?

A

~85% spontaneously resolve by 9 months of age

197
Q

Dx dacryocystocele

A

Nasal exam, nasal endsocopy, CT or MRI

198
Q

Rx for dacryocystocele

A

Endoscopic marsupialization (if presence of infection, respiratory obstruction, feeding difficulties) or Abx with excision for recurrent infected lesions (consider ophtho consultation)

199
Q

Pathophysiology of Thornwaldt’s cyst

A

Arises from a pharyngeal notochord remnant (pharyngeal bursa or pouch of Luschka)

200
Q

Location of Thornwaldt’s cyst

A

Nasopharynx (midline, surrounded by adenoid tissue)

201
Q

SSx of Thornwaldt’s cyst

A

asymptomatic, smooth mass found in nasopharynx; rare infection, postnasal drip, referred otalgia, or otitis media with effusion

202
Q

Dx of Thornwaldt’s cyst

A

CT or MRI, biopsy

203
Q

Rx for Thornwaldt’s cyst

A

Observation, Abx with marsupialization or excision for infected lesions

204
Q

What sinuses are affected the most in peds rhinosinusitis?

A

Typically involves maxillary and anterior ethmoid sinuses (sphenoid and frontal sinuses typically do not develop until 8-12 years old)

205
Q

Where is the larynx in an infant?

A

At level of C2-3, descends during infancy C6-7 by adulthood

206
Q

Where is the smallest cross-sectional area in infant and adults?

A

Infant is at subglottis (4-5 mm diameter in neonate), whereas in adult it is at glottis inlet (rima)

207
Q

unit decrease in subglottic stenosis results in

A

1 mm of subglottis edema in the neonate can reduce airway by more than 50%

208
Q

ETT size approximation

A

ETT size = (age + 16)/4

209
Q

3 weeks dev for respiratory primordium

A

thickening of foregut (primitive foregut) forming ventral laryngotracheal groove

210
Q

4 weeks dev for respiratory primordium

A

laryngotracheal groove evaginates to form the laryngotracheal diverticulum dividing the foregut into a dorsal (esophagus) and vental portion (larynx, trachea, lung) separated by the tracheoesophageal septum (incomplete fusion results in persistent lrayngopharyngeal or tracheoesophageal communication)

211
Q

5 weeks dev for respiratory primordium

A

larynx develops fro mmesenchymal swellings from sixth branchial arch with 3 tissue swellings (1 median swelling behind the hypobranchial eminence, which forms the epiglottis, and 2 lateral swellings that form the arytenoid cartilages) surrounding the laryngeal orifice

212
Q

6 weeks dev for respiratory primordium

A

Epithelial proliferation obliterates the laryngeal lumen

213
Q

8 weeks dev for respiratory primordium

A

larynx evident

214
Q

10 weeks dev for respiratory primordium

A

recanalization of larynx and trachea (no recanalization results in stenosis)

215
Q

Laryngeal branchial arch derivatives from arch II

A

lesser horn and upper portion of hyoid bone

216
Q

Laryngeal branchial arch derivatives from arch III

A

greater horn and lower portion of the hyoid bone

217
Q

Laryngeal branchial arch derivatives from arch IV

A

supraglottic structures (thyroid cartilage), superior laryngeal nerve (SLN) structures (cricothyroid muscle and pharyngeal constrictors)

218
Q

Laryngeal branchial arch derivatives from arch V/VI

A

glottic/subglottic structures (cricoid, cuneiform, corniculate, and arytenoid cartilages) and recurrent laryngeal nerve (RLN) structures (all intrinsic laryngeal muscles except the cricothyroid

219
Q

Esophageal embryology

A

Epithelial proliferation obliterates the lumen, recanalization occurs by 8th-10th week (abnormal recanalization results in congenital stenosis)

220
Q

Characters of stridor

A

Inspiratory stridor suggests supraglottic or glottic pathology, biphasic stridor suggests glottic or subglottic, expiratory stridor alone suggests distal tracheal or bronchial sourec

221
Q

Utility of AP and lateral neck x-ray in peds airway

A

Unilateral subglottic lesion (eg, hemangioma), subglottic narrowing (“steeple sign”), epiglottic widening (“thumb sign”)

222
Q

Utility of CXR in peds airway

A

Evaluate for foreign body aspiration (insp/exp CXR or lat decubitus film may demonstrate the foreign body and/or diaphragmatic flattening and mediastinal shift), other pulmonary causes

223
Q

Utility of CT neck/chest in peds airway

A

vascular compression

224
Q

Utility of MRI neck chest in peds airway

A

extrinsic compression, best for lymphovascular malformation work up

225
Q

What does L&B evaluate for in peds airway?

A

Evaluate for malacia (intrinsic or extrinsic), stenosis (location, length, etiology), fistulae and/or laryngeal cleft, masses or other lesions

226
Q

Cotton-Myer grading system for subglottic stenosis

A

Stage I: 1-50% obstruction
Stage II: 51-70% obstruction
Stage III: 71%-99% obstruction
Stage IV: no detectable lumen

227
Q

Indications for peds trach

A

Premature infants with cardiopulmonary or neurologic impairment requiring prolonged ventilator support
Upper airway obstruction, craniofacial anomalies
>2 kg

228
Q

Position of hyoid in peds trach

A

hyoid overlies superior laryngeal cartilage

229
Q

Peds trach technique

A

Small vertical or horizontal skin incision, stay sutures placed laterally through trachea on eitehr side of proposed vertical trachotomy incision (labeled “right” and “left”), tracheotomy incision most comonly at 2nd or 3rd tracheal ring, ICU until first trach tube change postop day 5-7

230
Q

Strategy for downsizing or decannulating trach tube

A

Endoscopy to eval for subglottic stenosis or suprastomal grnuloma

231
Q

Peds aerodigestive evaluation

A 
L&amp;B to eval for structural abnormality of aerodigestiev tract (eg larynegeal cleft, H-type tracheoesophageal fistula)
Flex bronch (bronchoalveolar lavage for cytology and microbio)
EGD with biopsy, pH impedance probe
232
Q

Surgical options of salivary management

A

If excessive sialorrhea and/or aspiration causing respiratory illness

  1. Botox: inject submandibular and parotid glands
  2. Submandibular gland excision and parotid duct ligation: severe cases (surgical rerouting of submandibular ducts also an option in patients who do not aspirate
233
Q

Etiology of congenital high airway obstruction syndrome

A

obstruction by congenital mass, eg teratoma, epignathus (teratoma arising from basisphnoid region and filling oral cavity; often protruding through the hard palate), lymphovascular malformation

234
Q

What is EXIT procedure?

A

Ex-utero intrapartum procesdure, where airway is secured at delivery while the patient is on placental circulation

235
Q

Most common cause of congenital stridor

A

laryngomalacia

236
Q

Pathophysiology of laryngomalacia

A

immature, constricted laryngeal anatomy with poor structural support and/or tone

237
Q

SSx of laryngomalacia

A

intermittent inspiratory stridor that may improve when prone
Exacerbated with feeding, crying, or when supine
Retractions, poor weight gain, FTT
Presents within weeks of birth
Normal voice
Usually self-limited and resolved by 18-24 months

238
Q

MC laryngeal findings on laryngomalacia

A
  1. Inward collapse of A-E folds, arytenoid cartilage, and epiglottis into laryngeal inlet during inspiration
  2. short aryepiglottic folds
239
Q

When is supraglottoplasty done for laryngomalacia

A

Release short A-E folds +/- remove excess mucosal tissue from arytenoids for severe dyspnea, failure to thrive, obstructive sleep apnea

240
Q

Etiology of congenital bilateral vocal fold immobility

A
  1. Neurologic
  2. Iatrogenic
  3. Idiopathic
241
Q

Which cause is most common for congenital bilateral vocal fold immobility?

A

Idiopathic

242
Q

What are the neurologic cuases for congenital bilateral vocal fold immobility?

A

Arnold-Chiari malformation and meningomyelocele

243
Q

What are the iatrogenic causes for congenital bilateral vocal fold immobility?

A

Birth trauma, increased risk with complicated or forceps delivery (traction injury, may be temporary)

244
Q

List some surgical options for vocal fold intervention

A

Lateralization, arytenoidopexy, arytenoidectomy, posterior cordotomy, posterior cricoid cartilage grafting, laryngeal reinnervation

245
Q

Location of congenital webs

A

MC anteriorly, thin or thick

246
Q

Pathophysiology of congenital webs

A

incomplete recanalization of the airway at 10th week of embryologic development

247
Q

Ssx of congenital webs

A

weak cry at birth, aphonia, variable degrees of respiratory obstruction (inspiratory or biphasic stridor)

248
Q

Dx for congenital webs

A

flexible nasopharyngoscopy, direct laryngoscopy

249
Q

Rx for congenital webs

A

genetics evaluation (eg, 22q11 deletion); endoscopic lysis +/- brief period of intubation or endoscopic keel placement, open lysis via laryngofissure with keel placement, may require tracheotomy

250
Q

Prognosis for congenital vs acquired stenosis

A

Congenital more likely to improve over time compared to acquired, and is frequently associated with syndromes (22q11 deletion, Down, CHARGE)

251
Q

Pathophysiology of congenital subglottic stenosis

A

incomplete recanalization; small diameter or elliptical cricoid cartilage (<3.5 mm diameter is abnormal); first tracheal ring partially telescoped under cricoid cartilage (trapped ring)

252
Q

Types of congenital subglottic stenosis

A
  1. Membraneous: circumferential, thickened mucous glands or fibrous tissue
  2. Cartilaginous: abnormal cricoid, trapped ring
  3. Mixed
253
Q

Type of stridor for SGS

A

biphasic stridor, retractions at rest

254
Q

DDx of SGS

A

croup, bacterial tracheitis, subglottic hemangioma, subglottic cysts, vocal fold parlaysis, complete tracheal rings

255
Q

When to do open surgical management for SGS?

A

For more severe or multilevel stenosis, endoscopic grade I-II failures, previous recon failures, hx difficult intubation, poor pulmonary function, sedation issues, medical comorbidities

256
Q

Types of open surgical intervention for SGS

A
  1. Expansion: anterior cricoid split, anterior cotal cartilage graft (single-stage, thyroid ala or costal cartilage), posterior cricoid split, posterior costal cartilage graft (posterior glottis stenosis, bilateral vocal fold immobility)
  2. Resection: cricotracheal resection (severe stenosis, previous airway recon, stenosis >3 mm from vocal folds)
  3. Slide tracheoplasty
  4. tracheotomy
257
Q

Etiology of congenital tracheal stenosis

A

Often due to complete tracheal rings

Associated with congenital cardiac abnormalities (eg, pulmonary artery sling)

258
Q

Tracheomalacia types

A

Intrinsic

Extrinsic

259
Q

Intrinsic tracheomalacia pathophysiology

A

Poor cartilaginous strength, low tone

260
Q

Comorbidities of intrinsic tracheomalacia

A

associated with premature infants with bronchopulmonary dysplasia (prolonged intubation and positive airway pressure) and tracheoesophageal fistula)

261
Q

SSx intrinsic tracheomalacia

A

failure to extubate, expiratory or biphasic stridor, barky cough, exacerbated with infection.
Usually self-limiting as cartilage stiffens with growth over years but may persist in children with tracheoesophageal fistula and a large pouch.

262
Q

Dx intrinsic tracheomalacia

A

history, flexible tracheoscopy, bronchoscopy (r/o tracheoesophageal fistula, laryngeal cleft)

263
Q

Rx intrinsic tracheomalacia

A

observation (typically resolves with growth), may require noninvasive ventilation, stenting (internal), splinting (external), tracheopexy or tracheotomy

264
Q

Types of vascular compression causing extrinsic tracheomalacia

A
  1. Double aortic arch
  2. Right aortic arch
  3. Anomalous innominate artery
  4. Anomalous left common carotid
  5. Left aortic arch with right descending thoracic aorta
  6. Pulmonary artery sling
  7. Retroesophageal right subclavian artery (dysphagia lusoria)
265
Q

Describe double aortic arch

A

Most common vascular anomaly to cause stridor.
right 4th brnachial arch persists
right aortic arch wraps around eosphagus and trachea

266
Q

Describe right aortic arch

A

right 4th branchial arch remains instead of left; association with tetralogy of Fallot in 30%
Types:
1. right aortic arch with aberrant left subclavian artery and left ligamentum arteriosum
2. right aortic arch with mirror-image branching and retroesophageal ligamentum arteriosum

267
Q

Describe anomalous innominate artery

A

left innominate originates more distally, innominate crosses over trachea from left to right

268
Q

Describe pulmonary artery sling

A

left pulmonary artery originates from right pulmonary artery, slings around right mainstem bronchus, then between trachea and esophagus
Associated with complete tracheal rings, tracheomalacia, and stenosis

269
Q

Describe retroesophageal right subclavian artery

A

Dysphagia lusoria. MC arch anomaly

Right subclavian artery originates as last branch from descending aorta

270
Q

SSx extrinsic tracheomalacia

A

biphasic stridor (external compression of trachea), barking cough, dyspnea with feeding, dysphagia

271
Q

Dx extrinsic tracheomalacia

A

bronchoscopy, barium esophagram, CT with contrast, MRA

272
Q

Rx extrinsic tracheomalacia

A

symptomatic compression requires surgical intervention

273
Q

Describe laryngeal cleft and laryngotracheoesophageal cleft

A

Failure of tracheoesophagela septum to develop

274
Q

SSx laryngeal cleft and laryngotracheoesophageal cleft

A

stridor, dysphagia, aspiration, recurrent pneumonia (mild clefts); respiratory distress at birth (severe clefts)

275
Q

Associations with laryngeal cleft and laryngotracheoesophageal clefts

A

Opitz G/BBB syndrome
Pallister-Hall syndrome
Tracheoesophageal fistula, esophageal atresia, laryngomalacia, congenital heart defects

276
Q

Dx laryngeal cleft

A

direct laryngoscopy +/- diagnostic laryngeal gel injection

Ancillary testing: MBSS to eval for aspiration, CXR

277
Q

Classification of laryngeal cleft

A 
Benjamin-Inglis classification
I: interarytenoid defect
II. incomplete cricoid involvemnt
III: complete cricoid invovelemtn
IV: below thoracic inlet
278
Q

Rx laryngeal cleft

A

goal is secure airway and avoid chronic aspiration
Symptomatic type I-II and certain type III clefts can be repaired endoscopically, most type III and all IV require open repair

279
Q

Pathophysiology of congenital tracheoesophageal fisulta

A

Failure of recannulation of the esophagus or developmental failure of teh tracheoesophageal septum

280
Q

Pathophysiology acquired tracheoesophageal fisulta

A

secondary to tracheostomy, long-term intubation, tumor, inflammation, trauma
Results in communication between lumen of the esophagus and the trachea

281
Q

Types of tracheoesophageal fistula

A

A. isolated esophageal atresia without TEF: second most common (~10%), associated with polyhydramnios
B. esophageal atresia with proximal TEF
C. esophageal atrea with distal TEF
D. esophageal atresia with proximal and distal TEF
E/H. Isolated tracheoesophageal fistula (H-type): rarely remains asymptomatic until later in life

282
Q

SSx of tracheoesophageal fisulta

A

immediate gagging and cyanosis after birth, gas-filled stomach
May present later in life wit cough, recurrent aspiration pneumonia, gagging
Long-term symptoms related to tracheomalacia and poor esophageal motility

283
Q

Dx of tracheoesophageal fistula

A

barium esophagram, bronchoscopy, esophagoscopy

284
Q

Rx for tracheoesophageal fistula

A

division (and reconstruction of the trachea/esophagus as needed)

285
Q

Causes of acquired glottic and subglottic stenosis

A

blunt trauma, endotracheal tube trauma, infection, caustic ingestion, foreign body

286
Q

SSx acquired glottic and subglottic stenosis

A

Inspiratory of biphasic stridor, dyspnea, cough

287
Q

Dx acquired glottic and supraglottic stenosis

A

flexible laryngoscopy, bronchoscopy

288
Q

Rx acquired glottic and supraglottic stenosis

A

endoscopic or open techniques depending on severity

289
Q

Causes of acquired subglottic and tracheal stenosis

A

Eight.

  1. endotracheal intubation
  2. postoperative
  3. granulomatous disease
  4. infectious
  5. idiopathic
  6. trauma
  7. systemic
  8. neoplasia
290
Q

Describe endotracheal intubation as a cause for acquired subglottic and tracheal stenosis

A

pressure necrosis results in ulceration and cartilage exposure, healing occurs by secondary intention causing fibrosis and stenosis

291
Q

Describe postoperative causes for acquired subglottic and tracheal stenosis

A

pressure necrosis from a high tracheostomy, cricothyroidotomy, or failed previous airway surgery

292
Q

Describe granulomatous disease as a cause for acquired subglottic and tracheal stenosis

A

TB (MC granulomatous disease of larynx), sarcoidosis, rhinoscleroma (klebsiella), granulomatosis with polyangiitis (Wegener’s)

293
Q

Describe infectious causes for acquired subglottic and tracheal stenosis

A

leprosy (epiglottic and vocal fold ulceration), syphilis, blastomycosis, coccidiomycosis, histoplasmosis

294
Q

Describe idiopathic causes for acquired subglottic and tracheal stenosis

A

amyloidosis, unknown

295
Q

Describe trauma as a cause for acquired subglottic and tracheal stenosis

A

foreign body, caustic ingestion, blunt trauma, hematoma, thermal injury

296
Q

Describe systemic causes for acuqired subglottic and tracheal stenosis

A

connective tissue disorders, GERD (presumed), radiation effects

297
Q

Describe neoplasia as a cause for acquired subglottic and tracheal stenosis

A

chondroma, fibroma, malignancy

298
Q

SSx for acquired subglottic and tracheal stenosis

A

dyspnea, biphasic stridor, cough, dysphagia, cyanosis, exercise limitation

299
Q

Dx for acquired subglottic and tracheal stenosis

A

Endoscopy, CT of neck, directed labs for various etiologies

300
Q

Rx for acquired subglottic and tracheal stenosis

A

Surgical management similar to congenital subglotitc stenosis (which is what)

301
Q

Risk factors for subglottic cyst

A

cause of stridor in a previously intubated infant (hx of prematurity and reflux)

302
Q

Rx for subglottic cyst

A

consider unroofing endoscopically with caterization of base; propensity for recurrence

303
Q

Causes for unilateral vocal fold immobility

A

birth trauma, intubation, PDA ligation, aortic arch anomaly repair, tracheoesophageal fistula repair

304
Q

What is the other word for croup?

A

acute laryngotracheobronchitis

305
Q

What ist he most common infectious cause of stridor in children?

A

acute laryngotracheobronchitis or croup

306
Q

Where does acute laryngotracheobronchitis most commonly affect?

A

subglottic region

307
Q

What viruses are implicated in acute laryngotracheobronchitis?

A 
Parainfluenza 1 (most common cause), 2, and 3
Influenza A, rhinovirus, repiratory syncytial virus, adenovirus, coinfection with multple viruses
308
Q

SSx of acute laryngotracheobronchitis

A

inspiratory of biphasic stirdor, gradual onset, long course (3-7 days), low-grade fever, relief in the recumbent position, brassy/barky cough (worse at night), hoarse, nontender larynx, no dysphagia, no drooling

309
Q

Dx for acute laryngotracheobronchitis

A

H&P, plain neck x-rays (steeple sign: narrowed subglottis on PA neck x-ray), flexible nasopharyngoscopy (not required)

310
Q

Rx for acute laryngotracheobronchitis

A
  1. Assess airway: intubation or tracheotomy rarely required unless there is co-existing laryngeal abnormality like SGS
  2. Medical management: humidified oxygen, corticosteroids, nebulized racemic epinephrine, Abx not required unless suspect bacterial superinfection
  3. Endoscopy: if no resolution with conservative management
311
Q

Other names for bacterial tracheitis

A

Exudative tracheitis

Membraneous laryngotracheobronchitis

312
Q

Pathophysiology of bacterial tracheitis

A

Bacterial superinfection following viral URI prodrome (Staph aureus)

313
Q

SSx of bacterial tracheitis

A

thick secretions in airway, fibrinous sloughing (exudative) membrane in trachea, high fever, tender larynx and trachea

314
Q

Dx of bacterial tracheitis

A

clinical suspicion, lateral neck x-ray may show shaggy appearance of trachea (membranes), flexible laryngoscopy may reveal exudative membranes in the subglottis and upper trachea, microlaryngoscopy and bronchoscopy

315
Q

Rx for bacterial tracheitis

A

aggressive pulmonary hygiene, parenteral Abx, microlaryngoscopy and bronchoscopy with membrane clearing and culture, may require intubation

316
Q

Can Diphtheria occur if vaccinated?

A

Yes. Milder form may present despite immunization

317
Q

Diphthreia pathogen

A

Corynebacterium diphtheriae

318
Q

SSx for Diphtheria

A

thick, gray-green plaques

Memranous, friable exudate on tonsils, pharynx, and larynx

319
Q

Rx for Diphtheria

A

airway management, laryngoscopy, isolation precautions, diphtheria antitoxin, antibiotics (PCN, erythromycin), humidity

320
Q

what is the other name for epiglottitis?

A

Acute supraglottitis

321
Q

Pathogen for acute supraglottitis?

A

classically Haemophilus influenzae b

Older children and adults may have infection with gram-positive bacteria

322
Q

Risks of acute supraglottitis

A

children >1 year old to adult (MC between 2-6 years old)

Rare since Hib vaccine

323
Q

Ssx of acute supraglottitis

A 
sudden onset (hours) and short course
High fever, odynophagia, dysphagia, droolin, dyspnea, "sniffing position" (neck hyperextended with chin protruding), no cough, mulffled voice, tender larynx
324
Q

Dx of acute supraglottitis

A

Clinical features, plain neck x-ray (thumbprint sign: swollen epiglotis on lateral x-ray)

325
Q

Complications of acute supraglottitis

A

bacteremia/sepsis, acute airway obstruction (death)

326
Q

Airway Rx acute supraglottitis

A

avoid aggravating patient and precipitating airway collapse (if high suspicion and symptomatic, establish airway in OR via intubation with preparation for trach)
DL with epiglottis cultures
For mild symptoms in stable patient with questionable diagnosis, consider plain x-ray, flexible laryngoscopy

327
Q

Medical Rx for acute supraglottitis

A

Monitored bed, parenteral antibiotics and corticosteroids for 7-10 days, extubation when clinical improvement and decreased epiglottic edema

328
Q

Locations of lesions of recurrent respiratory papillomatosis

A

wartlike, irregular, exophytic, between junction of ciliated and squamous epithelium (limen vestibuli, midzone epiglottis, ventricle margin, undersurface of true vocal fold)
Nasopharyngeal, tracheal, and bronchial lesions at sites of squamous metaplasia

329
Q

Types of RRP

A
  1. Juvenile onset <12 years, multiple sites, recurrent, may resolve spontaneously
  2. Adult onset >=12 years, may involve single site, recurrence less common, identical histology
330
Q

Complications of RRP

A

Rarely pulmonary involvement
Hemorrhage and abscess
Respiratory compromise

331
Q

Rx for RRP

A

Endoscopic: freq microlaryngoscopy and bronchoscopy with conservative excision employing cold techniques, microdebrider, lasers (KTP or PDL for anterior commissure)
Annual biopsy to r/o dysplasia
AVOID TRACH as may cause squamous metaplasi aand site for expansion
Adjunctive: cidofovir, interferon, retinoids, acyclovir, photodynamic therapy, bevacizumab

332
Q

Airway surgery and eosinophilic esophagitis

A

Implicated as a cause of airway surgery failure when uncontrolled

333
Q

SSx of eosinophilic esophagitis

A

feeding intolerance, failure to thrive, vomiting and abdominal pain, food impaction, rhinitis and rhinosinusitis, voice complaints, noisy breathing, reactive airway disease, aspiration, airway edema, SGS

334
Q

Dx of eosinophilic esophagitis

A

esophageal symptoms and characteristic histopathology of >= 15 eosinophils per high powered field in the absence of routine GERD or eosinophilia throughout the GI tract

335
Q

Rx for eosinophilic esophagitis

A

allergic treatments include oral corticosteroids, elimination diets, and immune-modulators

336
Q

MC non-food object in peds foreign body of esophagus

A

coins

337
Q

Most common location

A

cricopharyngeus

338
Q

Most common foreign body of the airway

A

Food including peanuts (MC)

339
Q

Dx airway foreign body

A

CSR with inspiratory/expiratory phases (evaluate for air trapping if object not radioopaque, object may produce ball-valve effect causing the affected side to be hyperinflated; atelectasis may cuase affected side to be hypoinflated)
Left/right lateral decubitus phases (affected lung may not undergo normal collapse when dependent), neck x-ray

340
Q

Caustic ingestion what is worse alkali or acidic?

A

Alkali agents pH >11.5, causes liquefaction necrosis (deeper penetration, more severe damage to the esophagus)
vs. coagulation necrosis (damage limited to the mucosa)

341
Q

Stages of esophageal caustic injury

A

<24 hours: dusky submucosal edema +/- ulceration
2-5 days: submucosal inflammation (gray coagulum) with thrombosis
5-7 days: sloughing of superficial layer
1 week: fibrosis of deep layers and formation of scars and strictures
2-5 weeks: contraction

342
Q

Assessment of injury after caustic ingestion

A 
Direct esophagoscopy required to evaluate esophageal and gastric injury (ideal 24-48 hrs), if performed too early (<12 hrs) may miss severity of dmaage, if performed >48 hours then esophagus too damaged risking perforation
Barium swallow (esophagram): first diagnostic tool >48 hrs; also obtain for progressive dysphagia to evaluate for stricture formation and to confirm perforation
343
Q

Types of esophgeal burns

A

First degree: superficial mucosal injury
Second degere: transmucosal injury:
Thrid degree: transmural injury

344
Q

Composition of branchial arch

A

composed of a cartilaginous bar, brachiometric nerve, muscular component, and aortic arch artery

345
Q

Composition of branchial groove or cleft

A

external, lined with ectoderm

346
Q

Composition of branchial membrane

A

formed between branchial groove and pouch

347
Q

Composition of branchial pouch

A

internal, linked with endoderm, contains a ventral and dorsal wing

348
Q

Name of branchial arch I

A

Mandibular arch

349
Q

Cartilage of branchial arch I

A

Mekel’s cartilage
Malleus head and neck, incus body and short process, anterior malleal ligament, mandible (formed from intramembranous ossification)

350
Q

Nerve/muscle of branchial arch I

A

CN V3.

Muscles of mastication, tensor tympani, tensor veli palatini, mylohyoid, and anterior digastric muscles

351
Q

Artery of branchial arch I

A

Maxillary artery

352
Q

What are hillocks of His of branchial arch I?

A
  1. Tragus
  2. Helical crus
  3. Helix
353
Q

Name of branchial arch II

A

Reichert’s cartilage
Manubrium of malleus, long process and lenticular process of the incus, stapes (except vestibular part of footplate), styloid procsess, stylohyoid ligament, lesser cornu and upper half of hyoid

354
Q

Nerve/muscle of branchial arch II

A

CN VII.

Muscles of facial expression, stapedius, stylohyoid, and posterior digastric muscles

355
Q

Artery of branchial arch II

A

Stapedial artery (degenerates; if too aerly causes microtia/atresia)

356
Q

What are hillocks of His of branchial arch II?

A
  1. Antihelix crus
  2. Scapha
  3. Lobule
357
Q

Cartilage of branchial arch III

A

greater cornu and lower half of hyoid

358
Q

Nerve/muscle of branchial arch III

A

CN IX.

Stylopharyngeus muscle, superior and middle constrictors

359
Q

Artery of branchial arch III

A

Common and internal carotid

360
Q

Cartilage of branchial arch IV

A

thyroid and cuneiform cartilage

361
Q

Nerve/muscle of branchial arch IV

A

superior laryngeal nerve.

Cricothyroid muscles and inferior pharyngeal constrictors.

362
Q

Cartilage of branchial arch V/VI

A

cricoid, arytenoid, and corniculate cartilage

363
Q

Nerve/muscle of branchial arch V/VI

A

recurrent laryngeal nerve

Intrinsic laryngeal muscle (except cricothyroid muscle)

364
Q

Artery of branchial arch V/VI

A

ductus arteriosus and pulmonary arteries

365
Q

Branchial cleft I

A

EAC, outer TM (dorsal part)

366
Q

Branchial cleft II

A

obliterates

367
Q

Branchial cleft III

A

obliterates

368
Q

Branchial cleft IV

A

obliterates

369
Q

Branchial cleft V

A

obliterates

370
Q

Branchial pouch I

A

eustachian tube, middle ear (mastoid air cells), inner TM

371
Q

Branchial pouch II

A

supratonsillar fossa, palatine tonsils, middle ear

372
Q

Branchial pouch III

A

epithelial reticulum of thymus, inferior parathyroids

373
Q

Branchial pouch IV

A

parafollicular cells (C-cells) of thyroid, superior parathyroids

374
Q

Describe thyroid embryology

A

Endoderm between the first and second branchial arch on the floor of pharynx (foramen cecum) invaginates around the 4th week and descends into mesencyhmal tissue along the path of the thyroid duct (anterior to the hyoid bone), forming a ventral diverticulum that differentiates at the distal end into the thyroid anlage
The proximal portion typically atrophies by the 6th week.

375
Q

Thyroid embryonic pathology

A

athyreosis (rare), ectopic thyroid (may be found anywhere along the thyroid duct from the tongue as a lingual thyroid to the sternal notch), thyroglossal duct cyst

376
Q

Describe parathyroid embryology

A

Third dorsal branchial pouch -> inferior parathyroids and thymus
Fourth dorsal branchial pouch -> superior parathyroids and C-cells of the thyroid

377
Q

Parathyroid embryonic pathology

A

Supernumerary parathyroids, aberrant parathyroids (most common location at the anterior superior mediastinum)

378
Q

What percent of peds head and neck masses are benign?

A

80-90% of pediatric H&N masses are benign

379
Q

DDx lateral neck mass

A

Congenital (branchial anomaly, laryngocele)
Inflammatory (lymphadenitis)
Vascular (hemangioma, lymphatic malformation, venous malformation)
Neoplastic (thyroid malignancy, thymic cyst, lipoma, neuroblastoma, lymphoma)
Traumatic (pseudotumor of infancy)

380
Q

DDx midline neck mass

A

congenital (thyroglossal duct cyst, ectopic thyroid, dermoid cyst, teratoma, thymic cyst)
Inflammatory (lymphadenitis, plunging ranula)
Neoplastic (thyroid malignancy)

381
Q

DDx submandibular mass

A

Inflammatory (plunging ranula, sialadenitis, lymphadenitis)
Vascular (lymphatic malformation)
Neoplastic (salivary gland neoplasm)

382
Q

PFAPA syndrome

A

Periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis, idiopathic condition in <5 years old, >=3 monthly episodes lasting 5-7 days that include fever/chills/malaise, pharyngitis, aphthous stomatitis, tender cervical lymphadenopathy

383
Q

Rx PFAPA syndrome

A

Corticosteroids in the acute phase and consider tonsillectomy

384
Q

Pathophysiology of branchial cleft anomalies

A

Developmental alterations of the branchial apparatus result in cysts (no opening), sinuses (single opening to skin or digestive tract), fistulas (opening to skin and digestive tract), or cartilaginous remnants

385
Q

SSx of branchial cleft anomalies

A

anterior neck mass (anterior to SCM, deep to platysma)
May have an associated subcutaneous palpable cord
Fistulas and sinuses may express mucoid discharge
Secondary infections (commonly after URI) cuase periodic fluctuation of size, tenderness, and purulent drainage
Cartilaginous remnants appear as small horns or firm bumps

386
Q

Dx branchial cleft anomalies

A

physical exam, CT w con, MRI, laryngoscopy to visualize internal opening if there are associated symptoms of if it will change the surgical approach

387
Q

Histopathology of brnachial cleft anomalies

A

Lined by squamous epithelium

388
Q

SSx first branchial cleft cyst

A

usually presents as a preauricular cyst (type I) or at the mandibular angel or submandibular region (type II)

389
Q

Pathways of Type I first branchial cleft cyst

A

Type I is ectodermal elements only; duplicated EAC
Typically begins periauricularly -> passes lateral (superior) to CN VII -> parallels the EAC -> ends as a blind sac near the mesotympanum

390
Q

Pathways of Type II first branchial cleft cyst

A

More common; ectodermal and mesodermal elements; duplicated membranous EAC and pinna
Presents near angle of mandible -> passes lateral or medial to CN VII -> ends near or in the EAC

391
Q

Rx for first branchial cleft cyst

A

Abx when secondarily infected (avoid I&D), full excision after resolution of infection (risk of facial nerve injury), may need superficial parotidectomy

392
Q

What is the most common branchial cleft abnormality?

A

Second branchial cleft cyst

393
Q

SSx second branchial cleft cyst

A

Cyst along anterior border of SCM

394
Q

Fistula pathway of second branchial cleft cyst

A

external opening at anterior neck -> along carotid sheath -> between external and itnernal carotid arteries -> deep to CN VII and superficial to CN XII and CN IX -> internal opening at middle constrictors or in tonsillar fossa

395
Q

Relationship between second branchial cleft cyst and second arch derivatives and third arch derivatives

A

the course of the second branchial cleft cyst runs deep to second arch derivatives and superficial to third arch derivatives

396
Q

Rx second branchial arch cleft

A

Abx when secondarily infected (avoid I&D), full excision after resolution of infection

397
Q

SSx third branchial cleft cyst

A

cyst in lower anterior neck (less common); majority on left side
Prsents as abscess neck mass (stridor, dysphagia, feeding difficulties), recurrent acute suppurative thyroiditis; often associated with thymic cysts

398
Q

Fistula pathway of third branchial cleft cyst

A

External opening at lower anterior neck -> superficial to CN X and common carotid artery -> superficial to CN XII -> deep to CN IX -> pierces thyrohyoid membrane staying above superior laryngeal nerve -> itnernal opening at upper (base of piriform sinus

399
Q

Rx for third branchial cleft cyst

A

Treat infection with Abx; full excision after resolution of infection, avoid I&D
Excision must include partial thyroidectomy (superior pole of affected side)
Endoscopic obliteration of the piriform opening increasingly popular

400
Q

Tell us about fourth branchial cleft cyst

A

Extremely rare; Ssx are similar to third branchial cleft cyst

401
Q

Fistula pathway of fourth branchial cleft cyst

A

external opening at lower anterior neck -> loop aroud CN XIII -> posterior to common carotid artery -> thoracic component with loop below the aorta (left) or around subclavian artery (right) -> posterior to thyroid gland -> tracheoesophageal groove -> pierces cricothyroid membrane beneath superior laryngeal nerve -> apex of piriform sinus; recurrent laryngeal nerve remains deep to tract

402
Q

Rx fourth brnachial cleft cyst

A

similar to third branchial cleft cyst, follow the tract

403
Q

Pathophysiology of thyroglossal duct cyst

A

familure of complete obliteration of thyroglossal duct (Creatd from tract of embryologic thyroid descent: from floor of embryologic pharynx [tuberculum impar], which later forms the foramen cecum, down to midline neck

404
Q

SSx thyroglossal duct cyst

A

midline neck mass with cystic and solid components, elevates with tongue protrusion (attached to hyoid bone), typically inferior to hyoid bone and superior to thyroid gland; may have fibrous cord, dysphagia, globus sensation

405
Q

Dx thyroglossal duct cyst

A

neck ultrasound (confirm presence of a thyroid gland; in 1% of cases, the TGDC contains the only functional thyroid tissue)

406
Q

Histopathology of thyroglossal duct cyst

A

lined with respiratory and squamous epithelium, possible thyroid follicles and colloid

407
Q

Complications of thyroglossal duct cyst

A

Rare malignant potential, secondary infection

408
Q

Rx for thyroglossal duct cyst

A

Sistrunk procedure (excision of cyst and tract, including cuff of tongue base and mid-portion of hyoid bone, 3% recurrence; without hyoid resection 20-50% recurrence)

409
Q

Define lingual thyroid

A

failure of thyroid gland to descend from the foramen cecum; presents as a posterior tongue mass, usually in females; in 75% it is the only functional thyroid tissue; potential malignant transformation

410
Q

SSx of lingual thyroid

A

dysphagia, dysphonia, stertor; frequently hypofunctioning

411
Q

DDx of lingual thyroid

A

thyroglossal duct cyst, lymphatic malformation, vallecular cyst, midline tumors (dermoid, teratoma)

412
Q

Dx of lingual thyroid

A

CT and/or neck ultrasound (identify caudal thyroid tissue), thyroid function tests, consider I-123 or technetium scan

413
Q

Rx of lingual thyroid

A

May observe if asymptomatic (watch closely for malignancy); ablative radioactive iodine considered in older adults; excision (transoral or transcervical) with possible thyroid tissue transplantation; almost all options require thyroid hormone supplementation or supplementation

414
Q

Pathophysiology of thymic cyst

A

remnant of third pharyngeal pouch between angle of mandible and midline neck

415
Q

SSx thymic cyst

A

unilateral (usually left) enck mass

416
Q

Dx of thymic cyst

A

biopsy, serum calcium (associated parathyroid disorders, DiGeorge syndrome/22q11, CT/MRI)

417
Q

Rx for thymic cyst

A

excision, may req thoracic surgery consultation

418
Q

Pathophysiology of dermoid cyst and teratoma

A

Derived from pluripotent embryonal stem cells

419
Q

Types of dermoid cyst and teratoma

A
  1. Teratoma: composed of all 3 embryologic layers
  2. Dermoid cyst: ectodermal and mesodermal elements only (MC)
  3. Teratomoma: differentiated to organ structure (usually fatal)
  4. Epignathi: differentiated to body parts (usually fatal)
420
Q

SSx dermoid cyst and teratoma

A

Soft midline neck mass, may be associated with tufts of hair

421
Q

Dx of dermoid cyst and teratoma

A

biopsy

422
Q

Complications of dermoid cyst and teratoma

A

rare malignant potential

423
Q

Rx for dermoid cyst and teratoma

A

excision

424
Q

What are the other names for congenital torticollis?

A

fibromatosis colli, sternocleidomastoid tumor of infancy, pseudotumor of infancy

425
Q

Pathophysiology of congenital torticollis

A

intrauterine or birth trauma causing muscle injury, hematoma, and resultant fibrosis (typically of the SCM)

426
Q

SSx of congenital torticollis

A

Presents 2-4 weeks after birth; head and neck held to diseased side, chin toward healthy side; firm thickened mass confined to SCM (may be tender)

427
Q

Dx of congenital torticollis

A

H&P (if biopsied looks malignant because of muscle cell death and regeneration with necrosis and mitotic figures)

428
Q

Rx for congenital torticollis

A

physical therapy, observation

429
Q

Lemierre’s syndrome

A

thrombophlebitis of the internal jugular vein following pharyngitis, PTA or suppurative lymphadenitis
Systemic microemboli leading to dyspnea and cough, pleuritic chest pain, pneumonia, arthralgia, endocarditis, meningitis, sepsis
Fusobacterium necrophorum

430
Q

Rx Lemierre’s syndrome

A

I&D; IV Abx for 3-6 weeks

Anticoagulation controvertial

431
Q

SSx atypical mycobacterial infection

A

slowly enlarging, nontender, indurated neck mass with progressiev skin discoloration (purplish), skin fixation, and possible fistulization
Common in anterior neck triangle and parotid region; corneal ulceration is the most common H&N manifestation
Does not cause pulmonary involvement but may colonize respiratory tract
Natural history is to suppurate and drain for 3 years then “burn out”

432
Q

Dx atypical mycobacterial infection

A

culture (req 2-4 weeks for growth), PCR, PPD (weak or negative)

433
Q

Rx atypical mycobacterial infection

A

triple antibiotic therapy (clarithromycin, rifampin, ethambutol for 6 motnhs)
Full surgicla excision vs I&D curettage

434
Q

What is the most common pediatric H&N malignancy?

A

lymphoma is most common pediatric malignancy of the H&N (excluding retinoblastoma and CNS malignancy)

435
Q

What are previous names of langerhans cell histiocytosis? What is it?

A

Histiocytosis X and reticuloendotheliosis

Noninfectious granulomatous disease

436
Q

Pathophysiology of langerhans cell histiocytosis

A

Granulomatous disease of unknown etiology, manifests as a proliferation of bone marrow-derived histiocytes

437
Q

Histopathology of langerhans cell histiocytosis

A

sheets of polygonal histiocytes, Birbeck granules (“zipper pattern), rod-shaped cytoplasmic organells with a central linear density and a striated appearance (“tennis-rackets”)

438
Q

What are types of langerans cell histiocytosis?

A

Eosinophilic granuloma
Hand-Schuller-Christian disease
Letterer-Siwe Disease
Congenital self-healing reticulohistiocytosis (Hashimoto-Pritzker syndrome)

439
Q

Define CHARGE syndrome

A

coloboma, heart disease, atresia, retardation, genital hypoplasia, ear anomalies

CHD7

Pasha (5 decks)

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