Upper Airway Obstruction

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Upper Airway Obstruction

• Presented by Pratibha Shirsat, M.D.

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Upper Airway Obstruction

• Infectious Causes of Airway Compromise
• Infection Super-imposed on Congenital Airway
  Abnormalities
• Trauma (Foreign Body)

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Unique Aspects of the Pediatric Airway

• Narrowest Part of the Airway-Cricoid Cartilage vs
  Glottis (Adults)
• Funnel Shaped Larynx
• Internal Anatomy-antero-caudal angulation of the
  vocal cords
• Many Complicating Factors
• 1. Relative Macroglossia
• 2. High Glottis
• 3. Slanting Vocal Cords
• 4. Narrow Cricoid Ring
• 5. Large Occiput
• 6. Narrow Airway minimal reduction in
  radiusairway resistance

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• Anticipation of the Difficult Pediatric Airway
• 1. Micrognathia (eg. Pierre-Robin sequence,
  Treacher-Collins Syndrome)
• 2. Macroglossia (eg. Downs Syndrome,
  Beckwidth- Wiedemann Syndrome)
• 3. Soft Tissue Infiltration (eg. Hunters,
  Hurlers, Ludwigs Angina)
• 4. C-spine Abnormalities (eg. Klippel-Feil
  deformity)
• Case presentation

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Clinical presentation of Upper Airway Compromise

• Dyspnea (trachypnea, grunting, nasal flaring)
• Stridor
• a. Inspiratory b. Expiratory c. Biphasic
• Wheezing
• Supraclavicular Retractions
• Drooling
• Positioning
• Dysphonia/voice changes
• CNS compromise

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Different Diagnosis

• 80 - infections
• 90 - Viral croup
• 5 - Epiglottits
• 5 - Other

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Croup Syndrome

• Laryngotracheobronchitis
• Spasmodic croup
• Bacterial tracheitis

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Laryngotracheobronchitis

• Epidemiology
• 15 of respiratory tract disease in pediatric
  practice
• Annual incidence 5 cases per year, 100 children
  during second year of life
• Seasonal variation- late fall early winter can
  manifest throughout the year
• B G
• Peak age 1 to 6 years

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• Etiology
• Parainfluenza 1,2,3
• 1,2, majority of out breaks
• Influenza A B
• Adenovirus
• RSV
• Measles
• Mycoplasma
• Most severe form influenza A
• Most mild form mycoplasma

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• Etiology-Bacterial Causes
• Secondary bacterial super infection
• Laryngotracheobronchitis and pneumonitis
• Strep pyogenis
• Strep pneumonia
• Staph auneus
• Hemaphilus influenzae
• Moraxella catarrhalis
• I.P. 2-6 days for viral croup

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• Pathogenosis
• Nasopharynx
• Resp epithelium of larynx and trachea
• Diffuse inflammation
• Erythema tracheall
• Edema Wall
• Impaired Vocal Cord motobility
• Subglottic trachea surrounded by firm
  cartilage (narrowist)
• further narrowing with inflammation

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• Of Tracheal Lumen
• Narrowing from fibrinous exudate and
  pseudomembrane
• Infiltration with histiocytes, lymphocytes,
  plasma cells, polynorphonuclear leukocytes
• Spasmodic croup
• Non inflammatory edema

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Clinical Presentation

• Viral prodome 1-3 days
• Rhinorrhea, pharyngitis, hoarseness barking
  cough
• 2) 3-5 days symptoms resolve or increase in
  severity with resp. distress

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Physical Examination

• Barking Cough/ Stridor
• Croup Score
• 0 1 2
• Inspiratory Sounds Normal Harsh./Rhonchi delay
  ed
• Stridor None Inspiratory biphasic
• Cough None Hoarse cry Bark
• Retractions/Flaring None Supraclavicular SC
  and IC
• Cyanosis (Sat
• CNS status
• a. Hypoxia-agitation
• b. Co2 retention-fatigue or agitation

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Laboratory Evaluation

• WBC 10,000
• Polys predominate
• High WBC count with left shift suggest bacterial
  superinfection
• X-ray of Neck Steeple sign
• Chest Xray Airtrapping
• pulmonary infitrate

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Spasmedic Croup

• Clinical signs
• 3 months to 3 yrs
• History of URI symptoms
• Awakens at night with sudden onset of dyspnea,
  cough
• Stridor no fever
• Resolves with mist or spontaneously

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Treatment

• Minimal stimulation
• Humidification
• Racemic Epinephrine
• a) constriction of subglottic mucosal and
  submucosal capillaries
• b) 0-6 months 0.25 ml 11000
• 6 months 0.5 ml

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• Mist 1) decreases viscocity of mucus
• 2) Soothes inflammed mucosa
• 3) Mist may activate
• mecharoneuptone that produce reflex slowing of
  resp flowrate
• Machanoreceptors

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• Steroids
• Decadron 0.6 mg/hg IM, IV, or PO
• Half life 36 to 42 hours
• Stabalizes capillary endothelial functions and
  lysosomal cell membrane.
• Inhaled steroids (Budoronide) not recommended in
  the USA
• Effective in 2 to 4 h.

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• Helium-Oxygen mixture
• Improve lamina gas flow because of low density
  and viscosity
• May be useful in avoiding intubation

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Intubation

• A. Rarely necessary in LTB. Even less with
  wider use of steriods
• B. Inability to maintain Sat 02 90 on 50 02
• C. Co2 retention and respiratory fatigue
• D. Use ETT size 9.5 less that predicted (16
  age)/4
• E. Intubation usually for 3-5 days
• F. Listen for development of airleak sign
  that edema is subsiding

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Epiglottitis

• Most dangerous airway infection in Pediatrid age
  group
• Infectious inflammation of epiglottis and
  arytenoid cartilage

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Epidemiology

• Mean age 4 yrs. 1 5 yrs.
• More common in winter and spring
• Marked reduction in incidence since HIB vaccine.

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Pathophysiology

• Organism most common
• 1). H. Fluenza, S. Aureus, GABHS, S. pneumo
• Bacterema seeding of epiglottis
  edema, hemorrhage and leudocyte
  infiltrate in subepithelial space of epiglottis
• Swelling of arydenoid cartilage
• Progressive obstruction of glottic opening

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Clinical Manifestations

• Sudden onset
• High fever
• a. Severe sorethroat and inability ot
  swallow
• b. drooling

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Physical Exam

• Toxic
• Sniffing position and drooling
• Muffled voice. Stridor4 less that in croup
• Dehydration
• Comparison of Epiglottitis versus Croup

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• Epiglottitis Croup
• Cause bacterial viral
• Age 2-7 yrs 1-4 yrs
• Obstruction supraglottic subglottic
• Onset sudden gradual
• Fever high low grade
• Dysphagia marked none
• Drooling present minimal
• Posture sitting recumbent
• Toxemia mod to severe mild
• Cough absent barking, brassy
• Voice muffled hoarse
• Resp. rate normal to rapid rapid
• Larynx palpation tender not tender
• Clinical course shorter longer

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Evaluation and Treatment

• Securing airway is the number one priority
• If epiglottitis is suspected, child should
  immediately be taken to OR.
• Intubation under controlled setting is crucial.
• Avoid invasive examination or procedures
• CBC, BC, ESR bacterial picture
• Endolateral Neck _at_ray thumbprint sign
• Artificial Airway required for all children
• a. Nasotracheal preferable over orotracheal
• b. Oxygen, antibiotics, fluid-rapidly reverse
  pathologic processes
• c. Extubation after fiberoptic evaluation of
  the airway shows edema (usually 16 48
  hours)
• 7. Antibiotics against H. Influenzae and S.
  Aureus

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Deep Neck Abscess

• 1. Six potential Spaces ?Airway Compromise
• I Submental
• II Sublingual
• III Submandibular
• IV Retropharyngeal
• V Parapharyngeal
• VI Peritonsilar

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• Superficial and Deep Fascia create spaces
• Deep layer further subdivided
• a. Superficial envelopes SCM and trapezius
• forms floor of
  submandibular space.
• b. Middle Surrounds viscera of neck
  (thyroid, larynx, trachea)
  continues into mediastinum.
• c. Deep Surrounds prevertebral muscles
  danger space etween alar layer
  and prevertebral layer

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Peritonsillar Abscess

• Epidemiology
• a. Accumulation of pus within the tonsilar
  fossa (pterygoid borders)
• b. More commonly seen in adolescents than
  younger children

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Etiology

• GABHS and Anaerogbes occasionally
• S. Aureus

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• History
• a. Trismus (irritation of Pterygoid
  muscles)
• b. Sorethroat and drooling
• c. May have hx of previous
  phargyngitis or present initially

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• Physical Exam
• a. Bulge in posterior Soft Palate
• b. Deviation of Uvula
• c. Halitosis and muffled voice
• d. Fever
• e. Toxic and Dehydrated

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• Evaluation and Treatment
• a. All Children should be admitted and
  treated
• b. Antibiotics ? Surgical drainage
• c. Greatest risk to airway Spontaneous
  rupture of abscess
• d. If child presents with significant airway
  compromise, may need to drain emergently
• e. Rarely require artificial airway but need
  to take great care with aspiration
  precautions

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Retropharyngeal Abscess

• Epidemiology
• a. Boundaries
• b. Generally seen in younger children (70 6 yrs of age)
• c. Associated with
• 1. Contiguous spread of infection (URI,
  tonsillitis, tooth infection)
• 2. Trauma (chicken bone, pencil)

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• Etiology
• a. Nasopharyngeal Aeorbes and Anaerobes
• 1. Streptococci, S. Aureus,
  Hemophilus, GABHS
• 2. Bacteroides, Peptostreptococci,
  Fusobacteria

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• 3. Physical Exam
• a. Toxic, possibly dehydrated
• b. Drooling in the absence of oral/pharyngeal
  findings
• c. May see bulgeof posterior pharyngeal wall
• d. Neck swelling/Torticollis
• e. Stridor generally a late manifestation
  rarely seen in children 3

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• Evaluation and Treatment
• a. Lateral Neck Xray widening of prevertebral
  space
• _ AP diameter . Diameter of vertebral
  bodies
• _ Loss of cervical lordosis
• _ Should be in extension and
  inspieratory film
• b. CT Scan / MRI definitive can help
  destinguis between early cellulitis and frank
  abscess
• c. CXR to R/O aspiration or mediastinitis
• d. Surgical Drainage
• 1. Still required in the majority of patients
• 2. If CT/MRI shows early cellulitis, can
  observe closely
• e. Antibiotics
• 1. Penicillinase resistant penicillin or 3rd
  Gen Cephalospoorin
• 2. Clindamycin or Metronidazole

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Complications of Deep NeckAbscesses

• Mediastinitis
• Internal Jugular Venous Thrombosis (IJVT)
• Carotid Artery Rupture
• Aspiration Pneumonia
• Meningitis

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Summary

• Variety of causes leading to upper airway
  emergencies in children
• Most commonly will encounter infectious causes
  and foreing bodies
• Need to classify childs airway as follows
• 1. Maintainable
• 2. Maintainable with Support
• 3. Not maintainable (Artificial Airway
  Required)

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• Consider unique anatomic aspects of the childs
  airway
• 1. Funnel shaped with narrow cricoid ring
• 2. Anterior displacement and angulation of
  vocal cords
• 3. High Glottis (larynx at C vs C- in adult)
• 4. Large Tongue and Occiput
• Anticipate difficult airways in children with
• 1. Micrognathia
• 2. Macroglossia
• 3 Soft Tissue Infiltration
• 4. C-Spine Abnormalities
• Once airway stabilized, can proceed with other
  diagnostic modalities