Airway Issues

8/12/2019 Airway Issues

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oan C. Arvedson, Ph.D.

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Airway Issues: StabilityCritical Basis for Oral Feeding

Joan C. Arvedson, PhD, CCC-SLP, BRS-S, ASHA [email protected] & [email protected]

DisclosuresI have the following financial relationships

relevant to the content of my presentation:

Cengage Learning: Royalties on sale of

books

Pearson: Royalties on sale of books

Northern Speech Services: Royalties on

sale of training manuals

I have no relevant nonfinancial relationships

to disclose

Education is the greatest

need of the people,

but first they must be fed

(Dantons Memorial, Paris)

Why Should We Try to Solve ComplexFeeding & Swallowing Issues?

Most infants & children have complexissues even if it looks simple superficially

Underlying physiologic stability critical basisfor oral feeding airway most important

Evaluation & intervention decisions musttake into account respiratory/airway status

Care a lot about kids & their families

Primary Needs for All Humans

Respiration/Airway

Nutrition/Hydration

Feeding, Swallowing & NutritionCenter at Childrens Hospital Parents/caregivers + child

Physicians (Gastroenterologists)

Nurses

Dietitians

Speech-Language Pathologists

Psychologists

Occupational Therapists

Scheduler-Coordinator


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Additional Specialties

Social Work

Physical Therapy

Otolaryngology

Pulmonology

Physiatrists (Rehab)

Developmental Pediatrics

Radiology

Cardiology

Surgery

Range of ServicesOutpatient clinic

Comprehensive evaluation

Follow-up based on individual needs

Outpatient intensive intervention 5 days

Inpatient intensive program

2 week admission parents with child

Psychologists initiate feedings, parentsobserve, brought in after a few days, thencoached with bug in ear

Close monitoring by dietitians & MDs

Dysphagia: Health Considerations

Pulmonary/airway issues

Nutrition/hydration & undernutrition

Neurologic & neurodevelopmental issues

Gastrointestinal (GI) tract issuesMedication effects

Airway/Pulmonary Focuses

Upper airway issues

Aspiration focuses later

Airway evaluation by non-physicians

Upper airway etiologies

Diagnostic categoriesAssessment

Intervention strategies

Bedside Airway Examination

Respiratory rate: at rest & feeding

Respiratory effort:

Stridor

Stertor

Retractions: suprasternal, substernal

Bedside Airway Examination

Vocal quality variables

Strong, clear phonation, appropriate pitch

Weak, breathy, husky to hoarse

Gurgly, wet

Velopharyngeal function inferences

(e.g., hypernasality, hyponasality)

Pharyngonasal backflow or reflux

Frequent burping or hiccups?


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Airway Stability for PO Feeding

Airway stability is prerequisite for successful PO

If airway concerns are noted during physical

exam, possible next steps:

Otolaryngology airway exam (FFL, DLB)

Bedside/clinical oral feeding evaluation

Combined FFL & FEES with ORL & SLP

Videofluoroscopic swallow study (VFSS)

Monitor status for a few days

Fixable Straight Forward Case:What & Where is the Problem?

Term C-section, poor progression of laborRespiratory distress at 1 hour of age

Transient tachypnea of newborn

Tonic-clonic seizures up to 30 sec, day 2

Head CT & EEG: normal

Feeding consult at 1 week of life

Upper Airway Obstruction

Feeding up to 1 hour for 1 oz with gagging,

choking, and gasping for air.

At rest, normal respirations

Neurodevelopmental exam normal

Feeding observation: good suck, inspiratory

stridor, & moderate chest retractions

Supraglottic airway obstruction suspected

What & where is the problem?

Next Steps in Examination

Lateral neck X-ray: Mass anterior to, but

separate from, epiglottis

FFL: Normal vocal fold movement

Mass noted in valleculae,

Partially occluding supraglottic larynx,especially with swallow

CT of nasopharynx: 1 cm2 soft tissue mass

Intervention for Vallecular Cyst

Surgical excision

Bronchoscopy no further abnormalities

Pathology benign cyst

Feeding no problems at discharge

Common Airway Problems withFeeding & Swallowing Difficulties

Choanal atresia or stenosis

Laryngomalacia

Midface & mandibular hypoplasia

Vocal fold paralysis or paresis

Laryngeal cleft

Subglottic stenosis

CNS & neuromuscular diagnosesaffecting airway protection


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Choanal Atresia

or Stenosis

Choanal Atresia

1 in 7,000 to 8,000 newborns, 50%-60%

unilateral

Usually presents with first feeding

Periods of cyanosis at rest, agitation,begins to cry, & breathes through mouth relieves airway obstruction

Some have little or no respiratory distress atrest, but major distress at onset of feeding

Choanal Atresia

Test for airflow: wisp of cotton created at

end of a cotton-tipped applicator

FFNL + CT scan of nose & nasopharynx

needed to determine type (bony, mixed, &

membranous ) & extent of lesion

Surgery in neonatal period, transnasal or,in some, transpalatal approach

Complication: GER with intermittent nasal

reflux (Beste, Conley, Brown, 1994)

Choanal or Nasal Stenosis

Deviated nasal septum rule out

Edema of nasal mucosa common with

nasal suction at birth clears when suction

stopped

Midnasal stenosis & anterior or nasalaperture stenosis may cause obstructive

problems & feeding problems

Choanal Stenosis: SLP Role

Stertor (nasopharyngeal noise due toobstruction) stethoscope not required

Unilateral stenosis can affect feeding:incoordination of suck, swallow, breathe

Check breathing when infant is quiet orasleep: Is mouth open? If yes, whathappens when you hold lips together?

Choanal Stenosis: Oral Feeding

Pacing may be sufficient with mild deficit

Nipple may have to be adjusted to allow

mouth breathing: best not to take it out

Try not to disrupt feeding

Monitor flow rate closely

Once nasal airway is sufficient & stable,

infant should feed well


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Beckwith-Wiedemann

Beckwith-Wiedemann Syndrome (BWS)

Macroglossia, omphalocele, ear creases,

& macrosomiaDevelopment can be normal

Mild to moderate MR reported in some

Feeding problems secondary to large

tongue that can block airway

Management varies: conservative to

surgery

BWS: Outcomes

Surgical techniques variable

Modified keyhole technique (Kaufman et al 08)

Submucosal minimally invasive lingual excision

(SMILE) (Friedman et al, 2008)

Radiofrequency reduction of tongue base (RFBOT)

Outcomes: VariableBest: Functioning tongue (normal mobility)

Worst: Tracheostomy (Kacker et al., 2000)

BWS: Outcomes

Decline in ability to detect salty & bitter

taste after tongue reduction (Matsune et al,

2006)

Reduction in apnea/hypopnea index

Improved speech in some

Laryngomalacia

Congenital Laryngomalacia (CLM)

Weak laryngeal tone

Prolapse of supraglottic tissue into airway

Common mechanisms

Cuneiforms drawn inward during inspiration

Exaggerated omega shaped epiglottis curlson itself

Arytenoid cartilages collapse inward


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CLM: Incidence & Presentation

Most common laryngeal anomaly

Affects up to 45% to 75% of all infants with

congenital stridor

Typical presentation

Inspiratory stridor within 1st 10 days of life

over months & peaks at 6-8 months

Most cases benign & resolve 12-24 months

Up to 22% severe major upper airway

obstruction

Stridor in Severe CLM

Inspiratory

High pitched

Loudest when upset

More evident in supine

CLM: Complications

Airway obstruction with cyanosis

Life-threatening apnea

Feeding difficulty with failure to thrive

Developmental delay

Pectus excavatum

Cor pulmonale

Cardiac failure

Asphysiation

Death

CLM with Other Conditions

Neurologic disease

Cardiopulmonary disease

Congenital anomalies

Syndromes

Other medical co-morbidities

CLM: Diagnosis

Respiratory & swallow evaluation

Flexible endoscopy (laryngoscopy)

Flaccid epiglottis

Poorly supported arytenoids

Short aryepiglottic folds

Tracheobronchoscopy may be used

Indirect laryngoscopy not usuallyused with infants

CLM: Etiologic Theories

First described 1843, etiology remains elusive

Anatomic: flaccid laryngeal tissue

Cartilaginous (chondromalacia): laryngeal

cartilage is abnormal, immature, & pliable

Neurologic: neuromuscular hypotonia most

commonly cited

GERD: implicated as causative factor, more

likely association


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CLM: Neuromuscular Etiology

Unclear whether alteration is neuromuscular or

located in PNS, CNS, or both

Sensorimotor integrative function or larynx

tested in 134 infants

Degree of alteration correlated with disease

severity

Sensorimotor integrative function improved as

symptoms resolvedThompson, 2007,The Laryngoscope

CLM: Feeding Difficulties

Gastroesophageal reflux likely a majorfactor

Secondary to upper airway obstruction

Incidence: 33% to 75%

Slow feeding, frequent emesis,

undernutrition

CLM: Range of Treatment

Mild: benign & self-limiting

Reassurance to parents

Follow-up

Severe: surgical intervention

Laser resection (Supraglottoplasty)

Management of GER

CLM: SLP Role for Feeding

Determine most efficient oral feeding:

position, liquid flow, pacing

Monitor inspiratory stridor & effect on PO

Effects of GER & nipple feeding?

Reassurance to parents re positiveprognosis in coming months

Spoon feeding & cup drinking may be

focus earlier than in typical infants

Midface & Mandibular

Hypoplasia

Midface Hypoplasia

Craniosynostoses most common

Crouzon

Apert

Autosomal dominant

Multiple anomalies: premature closureof cranial sutures,ocular proptosis dueto small orbits, cleft palate, finger &hand abnormalities in Apert


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Midface Hypoplasia: Management

Stridor at rest in severe forms (esp. no cleft)

Maxilla may be impacted against skull base

Less severe: oral feeding may stress amarginally compensated airway

Tracheostomy required in some

Midface advancement as young as 3 years,prefer to defer until after puberty

Mandibular Hypoplasia

Pierre Robin Sequence

Treacher Collins

Goldenhar

Hemifacial Microsomia

Mandibular Hypoplasia

All or part of mandible, bilateral or unilateral

Common malformation for infant respiratory

problems

Retrognathia/micrognathia

Glossoptosis

Cleft palate may exacerbate condition

Respiratory status improves with growth

Pierre-Robin Sequence

Mandibular Hypoplasia (micrognathia)

Glossoptosis (retroplaced tongue)

U-shaped cleft palate

80% per some current reports

Airway obstruction

PRS: Embryology

Abnormal mandible development

7 to 11 weeks PCA

High tongue position

Tongue cannot descend

Mechanisms variable

Pierre-Robin Sequence Types

True glossoptosis

Cleft portions of soft palate interposed

between tongue & PPW

Lateral pharyngeal wall hypotonia causing

hypopharyngeal collapse

Concurrent GERD/EERD may complicate


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Pierre-Robin Sequence

Associated Syndromes: 82%

Sticklers

22q11.2 deletion syndrome

(Velocardiofacial, Di George)

Treacher Collins

Miscellaneous

Non-syndromic: 18%

Stickler Syndrome

Pierre Robin SequenceSevere myopia

Retinal detachment, cataracts

Arthropathy (joint disorder)

Musculoskeletal abnormalities

Pinna malformations (10-12%)

Genetics Evaluation

Encouraged as part of newborn workup

Important to define possible syndrome or

additional anomalies as early as possible

Intervention strategies often depend on

accurate diagnosisPrognosis may be related directly to

underlying etiology

PRS: Upper Airway Obstruction

Most acute finding in infants

Not always due to glossoptosis

Usually immediate, may be delayed

Feeding difficulties related

Pulse oximetry monitoring

Feeding: Pierre Robin Sequence

Needs relate to degree of airway obstruction

PRS +/- Stickler syndrome

Feeding difficulties pre-intervention

Oral, pharyngeal, & esophageal phases

Non-oral supplements needed for prolongedperiods

Esophageal manometry: 50% abnormalities

Suggest brain stem control dysregulation

Baujat et al., 2001


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Feeding: Pierre Robin Sequence Tests related to swallowing efficiency

Electromyography:Sucking-swallowing incoordination

Esophageal manometry: Multipledisturbances in function

Interpretation: Dysfunction in motororganization of tongue, pharynx, &esophagus

Baudon et al., 2002

Growth Data

Deficient growth in PRS (Laitinen et al, 1994)

Premature birth

Associated anomalies

PRS with hypercaloric diet (Marques et al, 2004)

Improved nutrition status

Improved respiratory conditions (shorter

nasopharyngeal intubation)

Management of Airway for PRS

Nasopharyngeal Airway (NPA)

Mandibular Distraction Osteogenesis (MDO)

External distractors

Internal distractors

Tongue-Lip Adhesion (TLA)Periosteal release

Tracheostomy

Swallowing After MDO

Success relates to airway status, neurologic

status, & other medical/health variables

Timing of surgery (neonatal period vs

several months of age)

Gastrostomy tube for those who need

supplements for > 30 days

Prognosis: good for long term PO

PR Swallowing Disorders with MDO 18 patients, before MDO & 4 months after

Bilateral corticotomies, followed by distraction

External devices

Achieved 7 to 19 mm elongation (mean=12 mm)

GER in 83% associated with apnea episodes

Disappeared after MDO

Oxygen saturation 72% pre-op, 93% after

Apnea & hypopnea disappeared after distraction

Monasterio et al. 2004

PRS: Emphases in Treatment

Positioning

Feeding alterations

Intraoral prostheses not helpful

Thickened liquid be careful

If non-oral feeding for nutrition

Oral tastes as tolerated & safe

Not likely to be via nipple


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Vocal Fold Paralysis/Paresis

Vocal Fold Paralysis

Second most common congenitalabnormality of pediatric airway

VF in midline (adducted) in most cases

Good voice or cry, poor airway

Surgical goal: improve airway, while

maintaining normal voice & intact swallow

Vocal Fold Paralysis: Etiology

Bilateral abducted

Idiopathic or iatarogenic

Small subset: autosomal dominantlinked to chromosome 6q16.

Unilateral:S/p surgical procedures that may injure

recurrent laryngeal nerve

S/p traumatic event

Unilateral VF Paralysis: Management

May be asymptomatic or with signs relatedto laryngeal incompetence, e.g., aspiration& dysphonia

High % recover spontaneously

Collagen injection risk of aspiration &

improves vocal quality may avoidtracheostomy or GT

Patel, Kerschner, & Merati (2003).

Vocal Fold Paralysis: SLP Role

Voice evaluation

Breathy, dysphonic, excessive effort

FFNL for visual inspection

Feeding/swallowing evaluation

Instrumental examination

FEES

VFSS

Laryngeal Cleft


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Laryngeal Cleft: Epidemiology

Rare midline defect of posterior larynx &

membranous trachea

Usually present in newborn period

Incidence: 1/10,000 to 20,000 live births

No consistent pattern of inheritance

Typically present with airway obstruction

due to extra mucosa

Laryngeal Cleft: Basic Types

Type I: Above level of vocal folds involves

failure of interarytenoid muscle development

Type II: Extends into upper cricoid cartilaginous ring remains intact

Type III: Entire cricoid cartilage with orwithout extension into cervical trachea

Type IV: Extensive affectinglaryngotracheoesophageal structures.

Laryngeal Cleft: Diagnosis

Vital factors for diagnosis

High index of suspicion during clinical

exam or by history

Direct endoscopic exam under anesthesia

with specific palpation of arytenoidcartilage & interarytenoid space

Laryngeal Cleft: Clinical Signs

Coughing or choking

Cyanosis

Tachypnea

Recurrent pneumonia

Respiratory infectionRespiratory distress with oral feeding

Clinical Signs in Infants

GER may accompany & sometimes

adds confusion for diagnosis

Abnormal cry or stridor similar to

laryngomalacia

Laryngeal Cleftin Some Genetic Syndromes

Opitz (Autosomal dominant)

Hypertelorism, hernias, cardiac anomalies,

Laryngotracheal malformations + others

Pallister Hall (Single-gene malformation)

Bifid epiglottis

Central polydactyly (extra digits)

Hypothalamic hamartoma (benign tumor like

nodule


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VFSS Aid to Diagnosis

Suspicious, but not definitive

Pattern of aspiration not accounted for by

other oral or pharyngeal phase problems

Penetration appears between arytenoids

Definitive diagnosis

Direct laryngoscopy & bronchoscopy

Laryngeal Cleft: Management

Type I: may not need intervention

Injection (Cymetra) for some infants

Other types: Surgical correction

G-tube for feeding

Reconstruction after 1 year of age

Sooner if aspiration pneumonia with GT

feeds

Laryngeal Cleft Early Management

Usually NPO pre-op

Op: laryngotomy anterior approach

through thyroid cartilage

Expose area of cleft

Excise redundant mucosa

Two-to-three layer closure of cleft

Re-approximate anterior larynx

SLP Intervention

Non-oral stimulation to facilitate interest

in tastes & minimize defensiveness

Oral sensory issues

Oral motor skill development

Transition tube to oral feeding

Diet modifications, e.g., thickened liquid

may help short time with cautions!!

Postural changes

Laryngeal Cleft: Outcomes

Total PO variable time s/p surgery; somein 6 months

Possible complications

Fistula along suture line may needsurgery

Long-term tracheostomy that may affectvoice & speech output (speaking valvehelps some)

Subglottic Stenosis


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Subglottic Stenosis

Management of severe subglottic stenosisLaryngotracheal reconstruction

Cricotracheal resection

Posterior costal cartilage graft (with or

without vascular pedicle) usually preferred

over anterior approaches

Tracheostomy & Ventilator Issues

Related to Swallowing

Tracheostomy: Indications

Craniofacial abnormalities (13%)

Upper airway obstruction (19%)

Prolonged intubation(26%)

Neurologic impairment (27%)

Trauma (7%)Vocal fold paralysis (7%)

Carron et al., 2000

Tracheostomy: Inflated Cuffs

Prefer no cuff in pediatrics, if possible

Breathing in & out through tube only

No airflow through upper airway

Lack of phonation (no voicing)

Decreased sense of smell/taste

Risk of tissue necrosis

Esophageal impingement may cause GER

Tracheostomy: Aspiration Risk

Cuff of trach tube can tether larynx

Not elevate, epiglottis not tilt down

Lack of airflow through upper airway

Lack sensation in oropharynx

Lack sensation of pooled secretions

Vocal folds remain in open position

Tracheostomy: Aspiration Risk

Lack of subglottic pressure

swallow efficiency

effectiveness of cough resulting in more

frequent suction

physiologic PEEP (positive end-expiratory

pressure)

gas exchange due to surface area of alveoli

oxygenation

Atelectasis possible


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Tracheostomy: Speaking Valves

Normalizes pharyngeal, glottic& subglottic pressures

May facilitate

Improved pharyngeal sensation

Humidification, taste, & smell

Tracheostomy: Open Position Valve

Person must exhale to close the diaphragmof a speaking valve

Secretions travel up the tube & may

occlude the valve

Used for communication only

Patient Criteria for Use

Medically stable

Awake, responsive

Toleration of cuff deflation (partial?)

Gross aspiration/ventilator may prevent

Must be able to exhale sufficiently pasttracheostomy tube

Upper airway must be patent

Contraindications for Valve Use

Tube size that fills the trachea

Degree of stenosis &/or granulation tissue

(consideration of inhalation vs exhalation)

Foam-filled cuff

EdemaSecretions

Physiologic Benefits of P-M Valves

Improved voice production

Improved sense of smell/taste

Prevent aspiration (deflated cuff allows for

laryngeal elevation/excursion

Vocal fold closure airflow moves over

baroreceptors

Improved sensation of pooled secretions

Trial Use of Speaking Valve

Baseline measurements of oxygenation,

vital signs, breath sounds, color, work of

breathing, patient responsiveness

Assess upper airway patency

Deflate cuff (variable MD recommendations)

Vocalize on exhalation

Cough


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Treatment Strategies to FacilitateVocal Fold Function

Older child who can follow directionsHard glottal attack exercises

Vocal fold exercises to strengthen vfs

Verbal communication

Swallow evaluation & treatment

PT & OT exercises for overall strengthening

Tracheostomy: Feeding Problems

Restricted movement

Discomfort from tube

Incomplete glottic closure

Structural abnormalities of larynx

Reduced cough effectiveness

Feeding with Tracheostomy

Restricted laryngeal elevation

Infants less difficulty than older children

Blue dye testing why not?

Reason for tracheostomy may be factor

Degree of difficulty

Type of difficulty

Swallow Gains with Valve

Cuff must be deflated to aid laryngeal

elevation (Unless cuff not tight?)

Vocal folds closed

Restored airflow = improved sensation

Restored subglottic pressureImproved secretion management (cough

improved, suction less, reduced risk of

tracheal damage)

Valve Aids Tracheostomy Weaning

Physiologic benefits stated previously aid

in setting stage for weaning

Uses expiratory muscles

Restores normal physiology

Decannulation may occur sooner than

with no valve

Tracheostomy: Outcomes

Time to decannulation longer withneurologic impairment & prolongedintubation

Mortality 19% overall(3.6% tracheostomy related)

Deaths usually related to underlyingdisease, not tracheostomy itself

Carron et al., 2000


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Ventilator Management in NICU

Neurally adjusted ventilatory assist (NAVA)FDA approved therapy

Practical experience & data in this area

lacking

Carefully prepared & organized plan is

essential for successful implementation

NAVA: How it works

Allows synchronization of spontaneous

respiratory effort with mechanical

ventilation

Electrodes embedded within NG catheter

detect electrical activity of diaphragm &

transmit information to ventilator

Ventilator breath is triggered & terminated

by changes in this electrical activity

NAVA: How it works (cont)

Ventilator determines inspiratory pressure

in proportion to this electrical signal

Thus, patient determines respiratory rate,

tidal volume, peak inspiratory pressure,

mean airway pressure, & inspiratory &expiratory times

Valve Placement with Ventilator

Record ventilator settings (mode, rate, tidal

volume [VT], F1O2, PEEP, peak inspiratory

pressure [PIP], alarms)

Deflate cuff gradually

Monitor PIP for possible changes to VT

Ventilator Adjustments

Alarms (volume & pressure)

Compensate for loss of airflow

through vocal folds if necessary

PEEP on/off

Pressure vs flow trigger

Pressure support/pressure control

Ventilator Adjustments

PEEP

Pressure support

Humidification

Transition & troubleshooting

Anxiety & depression

Airway patency

Breathing pattern changes


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Valve Removal with Ventilator

Replace original circuit set-upReturn ventilator settings & alarms

to pre-valve parameters

Re-inflate cuff if that was baseline

condition

SUMMARY

Stable airway is a prerequisite for safe

oral feedingPulmonary deficits may cause or

exacerbate dysphagia

Dysphagia may cause or exacerbatepulmonary deficits/compromise

Professionals must understand airwayimplications to facilitate oral feeding

Documents

Airway Issues