Aspiration/Feeding and Swallowing Flashcards
Definition of Aspiration
Penetration of material below subglottic area and into the lower airways
2 types of aspiration syndromes
- Acute aspiration → may develop acute pneumonitis and possibly respiratory failure
- Chronic repeated aspiration → small volumes repeatedly aspirated → smouldering inflammatory state and eventual CLD
Consequences of aspiration
Large volume gastric content aspiration causes marked inflammation, airway edema, bronchorrhea and airway obstruction; if get to terminal respiratory units can get ARDS like picture
Nonvolatile lipid containing liquids (mineral oil) are not absorbable and aspiration results in persistent lipoid pneumonia, bronchiolar obstruction and chronic lung injury; for lipoid pneumonia BAL can be Dx and Tx
Repeat hospitalization/pneumonia
Bronchiectasis → respiratory failure
Causes of Aspiration
- Functional
- Swallowing dysfunction
- Crico-pharyngeal acalasia
- Esophageal dysmotility - Anatomical
- TEF
- Laryngotracheoesophageal cleft
- Laryngomalacia (+ neurovariant LM) - Neurologic
- Static encephalopathy
- Moebius syndrome
- Chiari malformation
- Vocal cord paralysis
Other: Swallowing dysfunction, GERD, Aspiration of saliva
Symptoms of Aspiration
Chronic cough, wheeze, congestion Choke/gagging with feeds FTT Apnea Intermittent fever Recurrent chest infections Wet vocal quality or wet breathing
Imaging findings in chronic aspiration
Centrilobular opacities
Bronchiolar obstruction ‘tree-in-bud’
Bronchiectasis
Steps in the swallowing process
Normal swallowing: requires intact anatomy and coordination of sensory and motor functions
Oral phase and pharyngeal phases
- oral = voluntary – chew food and deliver bolus to hypopharynx and then involuntary pharyngeal phase triggered and airway protection takes place (respiration is ceased, VC are adducted and closure of false VC and retroversion of epiglottis) and then many upper airway muscles facilitate bolus passage into esophagus
Swallowing develops early in fetal development (10-14wks) and the central pattern generation occurs at level of brainstem
Mechanisms of aspiration during swallowing
Breakdown in co-ordinated swallowing function
Delay initiation of swallowing → food enters hypopharynx before pharyngeal phase initiated and thus airway not protected
Inadequate airway protection from posterior larynx (ie. laryngeal cleft)
Impaired fuxn of upper a/w muscles (intrinsic laryngeal M’s)
Abnormal sensory function of upper airway/larynx (decreased laryngeal sensation)
Key points about swallowing dysfunction
Most often secondary to central or peripheral neurologic disease, functional immaturity or anatomic limitations; Most have some combo
Some children have no identifiable anatomic, neurologic or dev limitations (usually delayed initiation of swallowing)
Typically swallowing occurs in mid expiration, followed by deglutition apnea, followed by further expiration to prevent aspiration
▪ Often children < 6 months will swallow at end of inspiration and onset of
expiration
Newborn/pre-term particularly susceptible to aspiration
▪ Varied coordination
Infants may “tire out” at the end of a feeding session
Swallowing dysfunction in Neuro impaired child
Aspiration very frequent; may occur before, during or after swallow and often does not provoke cough clearance;
o may be secondary to poor oral prep, impaired laryngeal elevation, premature spillage of liquid, poor pharyngeal clearance and poor esophageal opening, decreased pharyngeal squeeze, fatigue
o Aspiration is the most common cause of death in these patients
Neuromuscular disorders: almost all have prolonged transit time, poor laryngeal elevation, decreased pharyngeal squeeze, persistent pharyngeal residue
Swallowing dysfunction in Peripheral neuro diseases
ex: VC paralysis (from surgery), congenital syndromes affecting CN function (CHARGE, Mobius etc), Chiari (from BS compression and impact on CN’s)
see dysphagia, aspiration, pharyngeoesophageal dysmotility, poor airway protection
Cricopharyngeal achalasia may be seen in Arnold Chiari Malformation (ACM) (failure of cricopharyngeal M to relax and impact upper esophageal sphincter to relax thus food cannot enter esophagus)
Swallowing dysfunction in Anatomic abnormalities
Can occur anywhere along aerodigestive tract and impact deglutition (craniofacial d/o ie. choanal stenosis, cleft palate, T21, PRS, neck cysts, tumors, vascular rings/slings, laryngomalacia etc) or if cause direct connection b/w airway and esophagus then may not impact deglutition (TEF, Laryngotracheoesophageal cleft - LTEC)
With Laryngomalacia, surgery can improve stridor and aspiration, however if supraglottoplasty can also make aspiration worse in some patients
Swallowing dysfunction in Tracheostomy
Many kids w/aspiration get trach for underlying medical condition and this impacts deglutition w/impared laryngeal elevation, alteration in timing and inability to increase intra-tracheal pressure
To help decrease aspiration in this population could use one-way speaking valve so they can increase sub-glottic pressure with swallowing
Ways to evaluate swallowing
- Clinical: SLP or OT (feeding behavior, aversion, oral motor skills)
- Radiographic
- VFSS
- FEES
Both are useful and equally sensitive at picking up aspiration; no real clear better test, may depend on patient
Key points with VFSS
- Improves clinical exam of swallowing
- Evaluates oral, pharyngeal, AND esophageal phases of deglutition
- Limited evaluation of anatomy
- Evaluates multiple consistencies
- Feeding recommendations made at time of study
- Widely available
- Radiation exposure
- Not portable, non-invasive
Key points with FEES
- Improves clinical exam of swallowing
- Blind to actual moment of swallow
- Does not evaluate esophageal phase
- Evaluates functional anatomy of swallow
- Evaluates airway protective ability and sensation
- Feeding recommendations made at time of study
- Not widely available
- No radiation
- Portable but invasive
- Good caregiver feedback
Relationship between GERD and Aspiration
well described relationship with GER and chronic respiratory symptoms such as: wheezing, chronic cough, nocturnal cough, apnea and recurrent pulmonary infections
- multiple possible mechanisms for GER-related respiratory symptoms, but clearly chronic aspiration of gastric contents does occur
Gastric contents contain acid, pepsin, bile and particulates that may play a role in pathophysiology of lung injury (not just low pH) → so acid suppression in itself, w/o reducing actual GER may not prevent CLI from GER-aspiration; also PPI’s increase bacterial colonization of gut
Risk of aspiration from GER increase in any of populations who have swallowing defect
Is the Lipid-laden macrophage index helpful in the assessment for GERD and aspiration?
Very inconsistent results between studies
- usually quote cut-off of 100
- no clear correlation between proximal reflux (acid/non-acid) and LLMI
- no clear role – may have ancillary role (my opinion)
Gastric pepsin seen to be high in tracheal aspirates in patients w/esophagitis and respiratory symptoms then those w/o esophagitis,
o Seems to be ubiquitously high in intubated babies and older intubated children and thus
may not be clinically useful biomarker of aspiration
o May indicate that GER aspiration is omnipresent in most intubated infants and children regardless of feeding status after a few days – not clear
Tx considerations for GER aspiration
Acid suppression does not reduce the number of reflux events, only pH of events
- PPI – useful for Tx of GER esophagitis, but re: aspiration, they do not decrease number of events
and encourage bacterial overgrowth and potentially higher bacterial load aspirated
- Pro-kinetics
Surgical options:
o Fundoplication – be careful in neuro impaired child as they may have more wretching and decreased efficacy of fundo; also if any esophageal dysmotolity you have to be very careful not to impede forward transit of food/secretions by fundo or you may worsen aspiration
o G-J or J-tube feeds – do not prevent reflux of gastric secretions, at risk of intussusception and displacement
▪ Can use GJ as a trial if the patient already has a G tube to see if there is improvement in symptoms
Aspiration of Oral Secretions - which populations?
Most neuro impaired kids who aspirate oral secretions do so because swallowing incoordination NOT excessive saliva
Patients with cricopharyngeal achalasia, esophageal dysmotility, diverticulum or stricture, however, likely pool secretions and aspirate at night time
Evaluation for Aspiration of Oral Secretions
Endoscopy with and w/o sensory testing probably best to directly visualize
Radionuclide salivagrams are performed and if see activity in trachea/bronchi confirms aspiration
o Can also use food colouring in children with trach, by placing it in buccal space a few times per day and having caregiver assess for presence of coloured suctioned secretions.
- neither one of these has been proven to be great test
Treatment of Aspiration of Oral Secretions
PO anti-cholinergic to decrease salivary production (AE: behavior changes, constipation, dry
mouth, urinary retention flushing, nasal congestion, vomiting, diarrhea) and may thicken secretions that could result in significant mucous plugging of a/w
o Use with caution in infants, children with neuromuscular disease, and those with small tracheostomy tubes
Salivary duct ligation/excision/botox (sub-mandibular most often instrumented) – all have shown to reduce drooling and decrease respiratory infections
o Parotid glands are major secretors in anticipation of eating - also commonly treated
Evaluation of Lung Injury caused by aspiration: Imaging
CXR – usually abnormal – hyperaeriation, segmental or sub-segmental infiltrates (usually not uniformly distributed), peribronchial thickening, findings usually in multiple lobes and dependent regions – these findings are no specific
- CT – tree-in-bud opacities, bronchial thickening, subsegmental atelectasis and bronchiectasis; not specific but if see multilobe-dependent distribution in child with clinical hx that fits, then likely aspiration
Ways to evaluate the Aerodigestive Tract
Once convinced there is chronic aspiration, you MUST search for a cause
- thorough assessment of upper a/w and GI anatomy: clinical exam, upper GI, bronchoscopy, upper
a/w endoscopy; rigid bronch for assessment of LTEC, H-type fistula and cricopharyngeal achalasia
GI endoscopy – trio endoscopy
If normal anatomical assessment, I think you need to assess for CNS causes (ie. ACM) and peripheral neuro causes
Functions of the larynx
- Connects upper and lower airways
- Closes during swallowing to protect LRT
- Generates sound for voice
Differences between child and adult in terms of upper airway
Positioned high in neck ~C1-3 (vs C6-7)
Thyroid cartilage rounded
Omega shaped epiglottis
Cricoarytenoid joints and vocal processes are relatively larger
Epithelium more prone to injury and stenosis
Small oral cavity relative to tongue (aids sucking)
Treatment/Management of Dysphagia
Direct rehabilitative exercises Sensory stimulation Alterations in positioning Specialized feeding equipment Behavioural approaches Supplementation of nutrition via NGT/GT
How do you produce a voice?
Vocal fold vibration requires the buildup of subglottal air pressure that overcomes the resistance of the partially adducted vocal folds.
Examples of Acquired and Congenital voice disorders in children
Related to use – nodules, puberphonia, paradoxical vocal cord dysfunction
Structure dysfunction – anterior webs, glottis and Subglottic stenosis
Recurrent papillomatosis
Neuromotor dysfunction – unilateral or bilateral VCP
GERD
Assessment of Acquired and Congenital voice disorders in children
History, examination Average fundamental frequency (F0) and intensity (I0) Frequency range Harmonics to noise ratio (HNR) Average air flow rate Estimated subglottic pressure Perceptual ratings of vocal quality Endoscopy
Management of Acquired and Congenital voice disorders in children
Surgical e.g. bilateral TVF paralysis, congenital web, congenital/acquired subglottic stenosis, papillomatosis
o Adequate expansion of the airway may preclude midline approximation of the TVFs
o Reconstruction of the voice following airway reconstruction may involve realigning the glottis or procedures to minimize glottis gaps
Vocal fold nodules
o Change traumatic phonetic behaviours
o Treat reflux, eosinophilic esophagitis, asthma, allergy – if present
Surgery
● Vocal cord cysts: Surgery with pre and post speech therapy
● Recurrent respiratory papilomatosis: Laser ablation, microdebridement, sharp resection, cautery ablation, tracheostomy
Behavioural Treatment for Acquired and Congenital voice disorders in children
Vocal behaviours
Resonant voice therapy – a technique that reduces laryngeal strain
Direct voice therapy techniques
Common concomitant (GI) disease in children with complex airway conditions
GERD, eosinophilic esophagitis (EoE), dysphagia, or disordered motility.
These children often have a history of prematurity and neurodevelopmental delay along with other attendant comorbidities associated with prolonged NICU admissions. They also may have syndromes.
Definition of Gastro-esophageal Reflex
Inconsequential transient return of gastric contents into the esophagus
Normal kids can have reflux into esophagus multiple times per day (half are non-acid)
Symptoms of GERD
Symptoms and/or mucosal changes related to excessive stomach acid regurgitation into the esophagus and or pharynx
Symptoms: RAD, chronic cough, hoarse voice, difficulty swallowing
Signs: laryngeal edema, cobble-stoning, mucosal erythema (nonspecific) acid reflux has been shown to decrease laryngeal sensitivity which could increase risk of aspiration
Path: mucosal sloughing, neutrophilic inflammation in alveolar tissue
Mechanism: GERD may be altered thoracoabdominal pressure that exists in children with obstructive airway disease may be a consequence rather than primary cause of asthma sx or exacerbations in CF
Sufficient concern that GERD might neg impact airway reconstruction surgery that empiric anti-reflux treatment is often prescribed
Diagnostic test for GERD
No gold standard test
● Clinical dx based on effortless regurg/heartburn
● Successful empiric trial of PPI
● Endoscopy – direct inspection and biopsy of mucosa to detect acid injury (controversy as to how to interpret finding as due to GERD)
● Multichannel intraluminal impedence plus pH-metry (MII-pH) – 24 hr study that measures frequency, duration/clearance, height of reflux and duration of acid exposure in the esophagus by means of a catheter placed via the nose
● Pepsin (gastric acid) in BAL – utility of this test yet to be determined
● UGI (barium) – not adequate to dx GERD as ingested contrast commonly refluxes back into the
esophagus even in normal kids
Treatment for GERD
Acid suppression: H2 antagonist, PPI
● Motility agent: Domperidone, Metoclopramide, Cisapride
● Surgery: fundoplication should be reserved for those that fail medical management
Side effects: gagging/retching, bloating, dumping syndrome (rapid gastric emptying when the undigested contents of your stomach move too rapidly into your small bowel causing abdominal cramps, nausea and diarrhea)
Examples of Disorders of Motility
- Esophageal dysmotility
2. Disorders of gastric emptying
Characteristics of Esophageal Dysmotility
Can be idiopathic but can also relate to nerve disruption after surgery (e.g. TEF repair or fundo)
Symptoms: inability to swallow, regurg, intractable GER symptoms
UGI= poor clearance of contrast in the absence of a stricture
Impendence testing can be used to evaluate antegrade esophageal emptying
Manometry shows diminished, absent, or even retrograde esophageal peristalsis
Treatment = supportive restrict bolus size, liquid formulas for most of calories, avoid fundo
Characteristics of Disorders of Gastric Emptying
Symptoms: nausea, early satiety, vomiting
Nuclear gastric emptying scan– can provide a quantitative assessment
Treatment:erythromycin as a prokinetic, botox to the pylorus, surgical pyloroplasty
What is Eosinophilic Esophagitis?
-Eosinophils are not normally in the esophagus but can be increased in variety of diseases – e.g. GERD, Celiac, Crohn’s, hypereosinophilic syndrome, eosinophilic gastroenteritis
To differentiate EoE vs GERD - failure to respond fully to acid suppression or by neg impendence study
EoE is a spectrum of conditions but most commonly a manifestation of allergic disease , mainly chronic Th2 hypersensitivity immune responses but can have IgE mediated features (e.g pos SPT to common food allergens)
M:F = 3:1; 2/3 have an atopic phenotype (asthma, eczema, food allergy); genetic predisposition
Symptoms: reflux symptoms, vomiting, feeding disorder, abdominal pain, dysphagia or food impaction
Definition of Eosinophilic Esophagitis
Defined as the presence of > 15 eosinophils/HPF on microscopic biopsy of the esophagus in the absence of GERD or any other condition that could promote eosinophilic inflammation
Can be patchy disease so recommend minimum of 5 biopsies
Pathology = thickening, furrowing of the esophageal mucosa, white plaques that are eosinophilic microabscesses on the surface (but 25% have normal appearance)
Treatment of Eosinophilic Esophagitis
Dietary antigen elimination
- Target offending antigen based on SPT
- Empiric elimination of 6 common food antigens:soy, milk, egg, fish, nuts, wheat
- Elemental formulas
Topical steroids
o Swallowed fluticasone or budesonide
Recommend repeat endoscopy to confirm histologic remission of the disease even if symptoms improve as chronic persistent eosinophilic inflammation associated with fibrosis and stricture development
