Aspiration Syndromes

Updated: Oct 24, 2022
Author: Cecilia P Mikita, MD, MPH; Chief Editor: Girish D Sharma, MD, FCCP, FAAP 



Aspiration syndromes include all conditions in which foreign substances are inhaled into the lungs. Most commonly, aspiration syndromes involve oral or gastric contents associated with gastroesophageal reflux (GER), swallowing dysfunction, neurological disorders, and structural abnormalities. The volume of refluxate may be significant, usually causing acute symptoms associated with the penetration of gastric contents into airways, or there may be episodic incidents of small amounts of oral or gastric reflux or saliva that enter the airways causing intermittent or persistent symptoms.

GER is very common in infants and children and has been associated with a spectrum of pediatric problems; however, the percentage of reflux that causes respiratory complications is unknown. In 1912, Sir William Osler described the relationship between asthma and GER by stating that "attacks may be due to direct irritation of the bronchial mucosa or... indirectly, too, by reflex influences from stomach." Recent literature describes GER and aspiration syndromes as common occurrences with increasing diagnostic rates. Swallowing dysfunction in conjunction with GER is more likely to cause respiratory symptoms than GER symptoms alone. Eosinophilic GI disorders (eg, eosinophilic esophagitis, gastroenteritis) may also manifest similarly to GER but are refractory to traditional reflux therapies.

Joint clinical practice guidelines for evaluation and treatment of GER in infants and children have been developed by The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN).[1]

Swallowing dysfunction is a known etiology of aspiration in children. Divided into 4 distinct phases, swallowing is a complex action that involves 5 cranial nerves and 26 muscles. The mouth, pharynx, larynx, and esophagus are involved in a coordinated effort to induce swallowing. Any anatomic, neurologic, or physiologic defect in the swallowing mechanism during the preparatory, oral, pharyngeal, or esophageal phases may lead to aspiration.

Cricopharyngeal dysfunction, cricopharyngeal incoordination of infancy, and transient pharyngeal muscle dysfunction are well described in the pediatric literature. Cricopharyngeal dysfunction involves cricopharyngeal muscle spasm or achalasia of the superior esophageal sphincter. Cricopharyngeal incoordination of infancy is noted in infants who have a normal suck reflex but have incoordination during swallowing; this is possibly secondary to delayed maturation of swallowing reflexes or may be associated with cerebral palsy.

Neurological disorders, including congenital and progressive diseases, may manifest as aspiration syndromes in infants and children. Isolated superior laryngeal nerve damage, vocal cord paralysis, cerebral palsy, muscular dystrophy, and Riley-Day syndrome (ie, familial dysautonomia) are a few of the neurological disorders associated with increased risk of aspiration.

Anatomic disorders, such as cleft palate, laryngeal cleft, esophageal atresia, tracheoesophageal fistula, duodenal obstruction, or malrotation, may have associated aspiration risk. Other conditions such as macroglossia, micrognathia, and laryngeal cleft may predispose patients to aspiration. Motility disorders, such as achalasia or connective-tissue disorders, are associated with increased risk of aspiration.

Studies in humans and animal models revealed that aspiration of acidic content (pH < 2.5) into the lungs causes mucosal desquamation, damage to alveolar lining cells and capillaries, and acute neutrophil inflammation.[2]


The act of swallowing is divided into the following 4 discrete phases: oral preparatory, oral propulsive, pharyngeal, and esophageal:

  • The oral preparatory phase begins when foods and liquids are placed into the mouth, mixed with saliva, and formed into a bolus.

  • The oral propulsive phase consists of moving the bolus into the pharynx, triggering the reflex swallow, which is the major component of the pharyngeal phase.

  • During the pharyngeal phase, the larynx elevates and closes at the level of the epiglottis, aryepiglottic folds, and true and false vocal cords. Normally, the laryngeal reflex during the pharyngeal phase of swallowing acts as a protective mechanism against direct or indirect aspiration.

  • The esophageal phase is initiated when the bolus passes through the relaxed cricopharyngeal muscle and enters the esophagus.

Aspiration may occur when foreign substances enter the hypopharynx, either before relaxation of the cricopharyngeal muscle or before closing of the laryngeal sphincters. In patients with neurological disorders that affect swallowing, the absence of a swallowing reflex within 30 seconds of the completion of the oral preparatory phase results in direct aspiration. Direct aspiration is the aspiration of a food bolus while swallowing, whereas indirect aspiration is the reflux of food from the stomach into the esophagus and pulmonary system.

Patients with structural abnormalities, such as H-type tracheoesophageal fistula, duodenal atresia, and achalasia, may have problems with direct aspiration, indirect aspiration, or both. Patients with H-type tracheoesophageal fistulas often aspirate pharyngeal secretions. If the fistula is distal, indirect aspiration of gastric contents is a risk. Patients with malrotation may have GER with associated aspiration risk.

GER is often caused by transient lower esophageal sphincter (LES) relaxation. Other mechanisms include a low resting LES pressure and increased intragastric pressure. Increased intra-abdominal pressure due to coughing raises the gastroesophageal pressure gradient and increases the risk of reflux. However, GER may be the etiology of chronic cough. This cause-and-effect relationship may be difficult to elucidate.

Several mechanisms, including the cough reflex, pulmonary macrophages, and the mucociliary escalator, are protective if aspiration occurs. If any of these actions are absent, impaired, or overwhelmed, chronic or acute aspiration symptoms may occur. The extent of injury is related to the amount and characteristics of the aspirate, the frequency of occurrences, and the effectiveness of protective lung-clearance mechanisms.

Model and Boysen reviewed the pathophysiology of pulmonary aspiration of stomach contents.[3]  Laboratory studies revealed that aspiration of significant amounts of gastric contents, regardless of the nature of the aspirate, causes acute respiratory insufficiency and chemical pneumonitis. Acidic refluxate with pH less than 2.5 appears to be the most caustic to the pulmonary system. Histologically, one may see damage to alveolar lining cells and capillaries, as well as bacterial invasion, mucosal desquamation, and mononuclear cell inflammation.

Respiratory symptoms due to aspiration of gastric contents may occur via several mechanisms. A vagally mediated reflex bronchospasm occurs in response to gastric acid irritation of the distal esophageal mucosa. Thus, reversible bronchospasm often occurs without documented indirect aspiration. Other potential mechanisms include heightened bronchial reactivity and microaspiration. However, as many as 70% of patients with pharyngeal dysphagia with aspiration have no obvious clinical signs of coughing, gagging, or choking. Chronic lung hyperinflation with flattening of the diaphragm decreases the protective reflux barrier of the diaphragm. An increased transdiaphragmatic pressure gradient predisposes to the movement of gastric contents into the esophagus.

Medications used to treat asthma may contribute to symptoms. Beta-agonists and methylxanthines decrease the LES tone. Aminophylline is known to increase gastric acid secretion. Angiotensin-converting enzyme (ACE) inhibitors and inhaled corticosteroids have been reported to cause chronic cough.

Apnea, obstructive and central, has also been associated with aspiration of gastric contents. Laryngospasm manifests as obstructive apnea secondary to reflux. Classically, obstructive apnea occurs within one hour after a feed when a patient suddenly stops, becomes apneic, stares, and develops a rigid opisthotonic posture. Continued ineffective respiratory effort is observed, but coughing or gagging is not necessarily present. If this progresses, pallor, cyanosis, and possible hypotonia ensue. The complete obstruction of the larynx impedes air movement, causing an obstructive picture. If incomplete laryngeal obstruction occurs, stridor may be noted during the examination. Central apnea has also been noted as a result of reflux. The superior laryngeal nerve has been implicated in this mechanism. Central apnea can be differentiated from obstructive apnea by the lack of respiratory effort observed.

Chronic inflammation of the larynx and subglottic space from recurrent aspiration may cause stridor and hoarse voice.


United States statistics

Medical practitioners are diagnosing GER and its respiratory complications more frequently now than in the past. Theories of the increased frequency of GER diagnosis include an increased prevalence of pathologic GER, improvement in diagnostic tests for GER, misdiagnosis, and overdiagnosis. The increase in diagnostic rate probably is multifactorial, but factors such as formula feeding, increased volume of feeds, and prolonged use of infant seating devices in infants too young to sit have been suggested as epidemiologic causes for this increase.[4, 5]

In a study of the diagnostic rate of GER in Army hospitals over a 25-year period (1971-1995), the total diagnoses of GER increased 20-fold, with 84% of cases in infants younger than 6 months.[6] The diagnostic rate for GER diagnosis rose from 0.74 in 1000 persons in 1971 to 8.16 in 1000 persons in 1995. Orenstein states that 40% of healthy infants regurgitate more than once a day, and as many as 20% of children reflux to the extent that parents feel it is a problem.[7, 8, 9] Nelson et al (1998) described that most infants outgrow this physiologic reflux but that as many as 5% of infants have persistent reflux symptoms.[10]

Approximately 7% of infants have reflux severe enough to be brought to a physician's attention. As many as 40-50% of infants with GER present with respiratory symptoms. Approximately 25-80% of children with asthma have GER,[11] but as many as one third of patients with pulmonary symptoms of GER have no esophageal symptoms.

Incidence of eosinophilic GI disorders has increased during the past decade. Eosinophilic esophagitis has been diagnosed in approximately 2 of 10,000 children in the Cincinnati region.[12] Another group of investigators noted that 1% of patients with esophagitis have eosinophilic esophagitis.

The incidence of swallowing dysfunction associated with aspiration syndromes is not known because clinical signs of aspiration may be quite subtle. As many as 70% of patients with pharyngeal dysphagia with aspiration have silent aspiration (ie, no overt clinical signs during aspiration). Sheikh et al published a retrospective review of 112 neurologically normal infants with chronic respiratory symptoms who underwent videofluoroscopic-modified barium swallow study. Almost 12% had evidence of swallowing dysfunction and silent chronic aspiration without evidence of gastroesophageal reflux.[13] . Laryngeal penetration visualized by videofluoroscopic swallowing has recently been associated with an increased incidence of pneumonia in children as compared to children with no evidence of penetration or aspiration.[14]

The incidence of aspiration syndromes associated with anatomic or neurologic disorders is unknown. The incidence of an isolated cleft palate is approximately 0.5 per 1000 live births, whereas the incidence of cleft lip and palate differs by ethnicity. Patients with a cleft palate are at risk for aspiration secondary to an abnormal communication with the nasal and oral cavities. Nasopharyngeal reflux commonly is observed in patients with cleft palate with or without associated cleft lip. Unilateral or bilateral vocal cord paralysis accounts for approximately 10% of all congenital laryngeal lesions. Esophageal atresia occurs in 1 per 3000-4000 live births, with 85% associated with tracheoesophageal fistulas. Patients with vocal cord paralysis and laryngeal clefts were noted to have increased incidence of laryngeal penetration and increased incidence of pneumonia and aspiration.[14]  

International statistics

International data on frequency of aspiration syndromes are not available.

Race-, sex-, and age-related demographics

In Whites, cleft lip and palate occurs in approximately 1 in 1000 births; in Asians, it occurs in approximately 2 in 1000 births. In Blacks, the incidence of cleft lip and palate is approximately 0.41 in 1000 births.

One study revealed an increased incidence of GER in males over females, but no strong prevalence in one sex has been observed. Cleft lip and palate are seen more commonly in males than in females, with approximately 60-80% incidence in males. Isolated cleft palates occur more frequently in females.

Physiologic GER (ie, benign regurgitation) occurs most commonly in the first few months of life but generally resolves by age 1-2 years. Approximately 84% of patients diagnosed with GER in Army hospitals in a 25-year period were younger than 6 months.[6] Patients with anatomic, physiologic, or neurologic disorders associated with aspiration are often diagnosed early. Esophageal atresia with or without tracheoesophageal fistula may be diagnosed in the delivery room or shortly after birth. The prevalence of respiratory complications of GER in infants and children by age is not known.


In general, the prognosis for an infant or child with an aspiration syndrome is good; but this depends partly on the underlying disorder. GER spontaneously resolves in most children by age 1-2 years.


Patients with an aspiration syndrome are at risk for severe respiratory sequelae and, possibly, death. Patients with a massive aspiration event have a mortality rate of 25%.[15]  One study by Kohda et al examined 72 infants with documented aspiration by fluoroscopy for etiology of the aspiration and prognosis.[16]  None of the patients without underlying neurologic disorders had evidence of aspiration after one year. In patients with neurological disorders, two thirds of patients had prolonged aspiration on follow-up. In patients who initially presented with a near-miss sudden infant death syndrome, or acute life-threatening episode (ALTE), 3 of 13 patients had prolonged aspiration.

No standard case definition of GER disease is recognized; thus, morbidity statistics are difficult to interpret. In 1959, Carre studied the natural history of severe GER and found that less than 5% of clinically affected patients died as a consequence of reflux.[17]


Chronic lung disease may develop from repeated aspiration of refluxate.

Pulmonary fibrosis may occur over time secondary to repeated aspiration of small volumes of gastric secretions, promoting a progressive fibrotic pulmonary response.

Chronic bronchitis and bronchiectasis are also recognized complications.

Patient Education

Educate patient and family regarding basic and conservative measures to prevent GER and ensuing complications.

For patient education resources from eMedicineHealth, see the Digestive Disorders Center, as well as Bronchoscopy.




Clinical signs of acute versus chronic lung aspiration can vary dramatically. Acute aspiration may manifest as coughing, wheezing, fever, and chest discomfort. In the setting of massive aspiration, the patient may present with cyanosis and/or pulmonary edema, which may progress to severe respiratory distress syndrome.[2] Occasionally, aspiration may be silent with no overt signs or symptoms.

The 4 syndromes that may be associated with chronic lung aspiration are recurrent wheezing, apnea, chronic cough, and recurrent pneumonia. Recurrent wheezing and asthma symptoms can be related to aspiration of gastric contents. Evaluate patients for aspiration who have asthma symptoms unresponsive to standard therapy; unexplainable or nocturnal symptoms; or whose symptoms are not associated with allergens, upper respiratory tract infection (URTI) symptoms, or exercise.

Recurrent pneumonia is often observed in infants who are neurologically challenged and in children who chronically aspirate who may be neurologically healthy. These children often have impaired airway protection mechanisms and are noted to both directly and indirectly aspirate. Apneic episodes, both obstructive and central in nature, may be associated with aspiration in young infants and children. Obstructive apnea secondary to laryngospasm is observed in infants who are awake or asleep.

Microaspiration from indirect reflux causes laryngeal inflammation and bronchorrhea, manifested as hoarseness and cough. Chronic cough, defined as a cough that lasts 3 or more weeks, may be the only manifestation of recurrent aspiration. Failure to thrive (FTT) is also associated with gastroesophageal reflux (GER) and can be caused by a wide variety of factors, including cystic fibrosis.

  • Patients often have a latent period after the aspiration event and the onset of symptoms. Symptoms usually occur within the first hour of aspiration, but almost all patients have symptoms within 2 hours of aspiration. Elicit a history of recurrent pulmonary symptoms from the parents and patient, including the following:

    • Wheezing, bronchospasm

    • Noisy breathing

    • Choking, gagging, coughing, and/or spitting during feeds

    • Recurrent vomiting

    • Apnea, bradycardia, cyanotic episodes

    • Recurrent stridor, hoarseness, sore throat

    • Chest discomfort

    • Unexplained nocturnal fevers

    • Night sweats

    • Purulent sputum

    • Chronic cough (at least 4 wk in duration)

    • Nocturnal wheezing or cough

    • Excessive salivation

  • Other associated findings or conditions include the following:

    • Failure to thrive (secondary to calorie wasting)

    • Apnea and bradycardia (especially in young infants)

    • Hiccups

    • Recurrent episodes of pneumonia or bronchitis

    • Cystic fibrosis

    • Bronchopulmonary dysplasia

    • Pulmonary abscess

    • Pulmonary fibrosis

    • Bronchiectasis

    • Chronic bronchitis

    • Obliterative bronchiolitis

    • Interstitial lung disease

    • Other chronic lung diseases

Physical Examination

Physical findings may include the following:

  • Dysmorphic features (cleft palate, micrognathia, macroglossia)

  • Fever

  • Tachypnea

  • Heterophonous wheezing versus homophonous wheezing: Heterophonous wheezing is noted with small airway obstruction, whereas homophonous wheezing is noted with central airway involvement

  • Crackles

  • Noisy breathing

  • Cough (characteristics, timeframe, triggers)

  • Congestion

  • Clubbing associated with chronic lung disease

  • Increased work of breathing; grunting, flaring, retractions

  • Cyanosis

  • Hypoxemia

  • Weak suck

  • Shock

  • Stridor

  • Hoarse voice or cry

  • Irritability

  • Excess drooling

  • Dental erosions

  • Globus hystericus





Laboratory Studies

Laboratory studies in a thorough evaluation should include the following:

  • CBC count with manual differential

  • ABG or pulse oximetry

  • Sweat chloride

  • Pulmonary function test

  • Serum immunoglobulin G (IgG), immunoglobulin M (IgM), immunoglobulin A (IgA), and immunoglobulin E (IgE) levels (possibly)

Skin prick testing, allergen-specific serum IgE, and/or food atopy patch testing to common foods may be performed if eosinophilic esophagitis is considered in the differential diagnosis.

Imaging Studies

Chest radiography may reveal hyperinflation; marked diffuse interstitial or perihilar infiltrates, unilateral or bilateral; peribronchial thickening; pleural effusion; lobar or segmental consolidation; bronchiectasis; or atelectasis. See the images below.

Chest radiograph of a child with a tracheostomy an Chest radiograph of a child with a tracheostomy and recurrent aspiration reveals patchy infiltrates and increased interstitial markings.
Lateral chest radiograph of the same child as in t Lateral chest radiograph of the same child as in the previous image reveals increased interstitial markings and patchy and perihilar infiltrates.

High-resolution chest CT scanning may reveal bronchial thickening, bronchiectasis, ground-glass opacities, tree-in-bud centrilobular opacities, and air trapping.

Barium esophagram is used to evaluate for anatomic or physiologic abnormalities of the upper GI tract, to quantify the degree of aspiration during swallowing, and to assess texture-specific foods and swallowing. Anatomic abnormalities, including a hiatal hernia, malrotation, pyloric stenosis, and antral or duodenal webs, may be diagnosed and may predispose an individual to gastroesophageal reflux (GER). These tests are neither sensitive nor specific in the diagnosis of GER.

Gastroesophageal scintigraphy, is a radionuclide study that provides a more functional or physiologic assessment for GER and aspiration. Food of formula labeled with a radionuclide is introduced and the patient is scanned for evidence of reflux and aspiration for one hour. This test also lacks sensitivity and specificity in the diagnosis of pathologic GER.

A study by Fiori et al suggests that lung ultrasonography may be a feasible method to detect lung aeration abnormalities, possibly related to aspiration during meals, in infants with neurologic disorders. Thirty-five infants (mean age 20.2 months) with cerebral palsy or other encephalopathies were included in the study. Lung ultrasonography revealed meal-related abnormalities in infants with neurologic disorders, whereas no significant abnormality was found in a sample of typically developing control subjects.[18]


Procedures used in the workup of aspiration syndromes include the following:

  • Pulse oximetry

  • Videofluoroscopic swallow study (VFSS) and fiberoptic endoscopic evaluation of swallowing (FEES): VFSS is the criterion standard for assessing the 4 phases of swallowing using various consistencies of barium or food. FEES may be used to assess the oral and pharyngeal phases of swallowing only. The VFSS and FEES are often complementary studies in the assessment. Visualization of entry of material below the true vocal cords is a clear risk factor for aspiration pneumonia. Penetration of material into the laryngeal vestibule but not below the true vocal cords may be a risk factor for aspiration pneumonia as well.  Recommendations for determining compensatory swallowing strategies and liquid consistency can be made based on the results of the VFSS and/or FEES.

  • Fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) with staining for lipid-laden macrophages: Some have found evaluation for pepsin in BAL fluid to be helpful.

  • Esophageal pH monitoring for 24 hours: This is a reliable measure to evaluate acid reflux, but the level may be normal in some patients with GER and the test does not document nonacid reflux. Multichannel intraluminal impedance and pH monitoring (MII-pH) may detect anterograde and retrograde passage of refluxate, irrespective of pH. This can measure both acid and nonacid reflux and evaluates the change in intraluminal electrical resistance that occurs with advancement of a bolus. Normal values for impedance have not been established for pediatric age groups.

  • Esophagogastroduodenoscopy (EGD) with biopsies to assess eosinophilic infiltration: GER disease may be represented with distal esophageal erythema, erosions, ulcers, and mucosal friability. Characteristics of eosinophilic esophagitis include linear furrowing, mucosal granularity, scattered exudates, and concentric esophageal rings. A normal appearance of the esophagus does not exclude eosinophilic esophagitis and biopsies are recommended when endoscopy is performed.

  • Radionuclide salivagrams: These may be used in patients with possible salivary aspiration.

  • Immunocytochemical staining of alveolar macrophages for milk proteins (experimental)

Histologic Findings

Bronchoscopy may reveal airway mucosal desquamation, mononuclear cell inflammation with granuloma formation, bacterial invasion, and cell damage.

Lipid-laden macrophages may be identified with oil red O stain on bronchoalveolar lavage samples. This may be an indicator of aspiration by the sensitivity and specificity is poor.

Eosinophilic esophagitis can be distinguished from GER if the inflammatory infiltrate has more than 15 eosinophils per high-power field in one or more biopsies, eosinophils are isolated to the esophagus, and the patient was on a proton-pump inhibitor for at least 6 weeks.



Medical Care

Conservative therapy is the initial treatment of choice to prevent aspiration syndromes and often results in significant improvement in respiratory symptoms. Position infants in the prone or upright position. Avoid placing infants younger than 6 months in a seated position for approximately 90 minutes after a feed. Do not feed the infant within 90 minutes before bedtime. Elevation of the head of the bed approximately 30° may help, although young infants may slide down the bed during the night. Dietary modifications include thickening feeds for infants; breastfeeding; decreasing volume of feeds (10-20 mL/kg per feeding); and feeding small, frequent meals. Patients with swallowing dysfunction may benefit from certain food consistencies, positioning, and adaptive feeding equipment or utensils.

The management of an acute aspiration event consists of conservative management, observation, and possible antibiotic therapy. Initially, the patient's upper airway should be cleared and endotracheal intubation should be considered if the patient is unable to protect his airway. Close monitoring in an inpatient setting is recommended for at least 48 hours. Initially, empiric antibiotic therapy is not recommended, even if fever, clinical, laboratory, or radiographic findings are present. Selection of resistant organisms with the use of empiric, broad-spectrum antibiotic therapy is always a concern, especially in an uncomplicated chemical pneumonitis picture. If the patient fails to improve after 48 hours, the addition of broad-spectrum antibiotics is recommended.

A second or third generation cephalosporin is appropriate to cover potential gram-positive flora from the oropharynx and gram-negative organisms from the GI tract. Anaerobic coverage is not routinely required initially. Limited and controversial data on the role of corticosteroids in the management of acute aspiration events are available. Numerous animal studies and clinical trials fail to demonstrate a significant beneficial effect of corticosteroids after acute aspiration events. Based on these data, routine administration of systemic corticosteroids is not recommended.

Patients should be seen by their primary care manager for routine well-child visits and regularly for follow-up care.

Admit infants and children with aspiration syndromes if a documented oxygen requirement is noted, if the patient has altered mental status, or if adequate medical care is unable to be met in the outpatient arena.

Admit to the intensive care unit if the patient requires intubation, shows signs of impending respiratory failure, or shows instability on the ward with requirement of closer monitoring.

Conservative measures are the best deterrence against gastroesophageal reflux (GER). Attention to feeding volumes, positioning, and encouragement of breastfeeding may be helpful to decrease GER signs and symptoms in infants.

Surgical Care

The American Gastroenterological Association has published clinical practice guidelines regarding surgical intervention for oral pharyngeal dysphagia.

Surgical management with Nissen fundoplication and/or gastrojejunostomy is generally not first-line therapy for gastroesophageal reflux (GER) lung disease but may be appropriate for some individuals with neurological impairment or patients with respiratory complications or recurrent aspiration that have failed medical therapy.[1, 19] Surgical treatment of curable anatomic disorders, such as malrotation, is paramount. A systematic review of the surgical treatment of gastroesophageal reflux disease reported that fundoplication did not affect the rate of hospitalization for aspiration pneumonia or apnea.[20]

Patients who are neurologically impaired, have GER, and require a feeding tube are usually initially treated with fundoplication and gastrostomy. However, a percutaneous endoscopic gastrojejunostomy may be an intermediate step before surgical intervention.

Several surgical procedures have been tried as an adjunct to fundoplication and gastrostomy to prevent direct aspiration. Total laryngectomy, glottic closure, tracheostomy, and injection of Teflon into the vocal cords have all been tried in patients with persistent direct aspiration.

Laryngotracheal separation, with or without end-to-side laryngoesophagectomy, has been tried more recently in children with neurological impairment who have intractable aspiration pneumonia as an adjunct to fundoplication and gastrostomy.[21] In this procedure, the larynx and trachea are permanently divided; therefore, aspiration can never occur, but phonation is sacrificed.


A primary care provider can successfully provide routine medical care for children with aspiration syndromes.

Consultation with a speech-language pathologist or occupational therapist is recommended to assess swallowing dysfunction. Oral structure and function, clinical signs of safe swallowing, and positioning should be assessed. Compensatory feeding strategies should be implemented to protect the airway.

Refer patients to a pediatric pulmonologist and/or pediatric gastroenterologist if the patient does not respond to conservative or simple medical therapy or if the ordered studies are equivocal.

A pediatric neurologist should thoroughly evaluate patients with possible neuromuscular disorders.

A pediatric allergist/immunologist and/or pediatric gastroenterologist should be consulted if eosinophilic esophagitis is considered.

Diet and Activity


Several dietary modifications can be initiated to decrease the risk of aspiration. Restricting fluids, decreasing volume and increasing frequency of feeds, breastfeeding, providing texture-modified diets, thickening feeds, and not feeding within 90 minutes of nap or bedtime may decrease GER and aspiration. Infants who are breastfed are less likely to have GER than formula-fed infants.[22]

Special feeding equipment or utensils and positioning may also help patients with swallowing dysfunction or anatomical defect.

In certain cases, transpyloric feedings may be necessary to decrease the risk of aspiration.

In addition, avoidance of certain foods (eg, caffeine, fatty meals, carbonated beverages, peppermint, citrus) may decrease GER in older children and adults. Other nonpharmacologic measures for older children and adults include weight reduction for persons who are overweight and avoidance of overfeeding, active/passive smoking, alcohol, and food consumption before bedtime.[22]

If the volume of aspiration is greater than 10% of the bolus feed, enteral feeds may not be appropriate.


Simple modifications in activity help decrease incidence of physiologic and pathologic GER.

Elevation of the head of the bed approximately 30° and avoidance of seated devices for approximately 90 minutes after feeding may decrease GER and aspiration.

Avoidance of prolonged use of seated devices in very young infants may be beneficial.



Prokinetic agents

Class Summary

These agents are used to augment cholinergic activity and to improve motility in the GI tract.

Metoclopramide (Reglan, Clopra, Maxolon)

Increases resting esophageal sphincter tone, improves gastric tone and peristalsis, relaxes the pyloric sphincter, and augments duodenal peristalsis with the net effect of increasing GI motility and decreasing reflux potential. Dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. Acts centrally on chemoreceptor triggers in the floor of the fourth ventricle, which provides important antiemetic activity.

Bethanechol (Urecholine)

Cholinergic agent that increases tone, amplitude of contractions, peristaltic activity, and secretions of the GI tract.

Histamine (H2) receptor antagonists

Class Summary

These agents do not reduce the frequency of reflux but decrease the amount of acid in the refluxate by inhibiting acid production. All are equipotent when used in equivalent doses and work best in nonerosive esophagitis. Because of the superiority of proton pump inhibitors (PPIs), H2 blockers may be reserved for use in patients unable to tolerate PPIs.

Cimetidine (Tagamet)

Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Ranitidine (Zantac)

Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Proton pump inhibitors

Class Summary

These agents act by blocking the enzyme system responsible for active transport of protons into the GI lumen (ie, hydrogen/potassium adenosine triphosphatase [H+/K+ ATPase]) of the gastric parietal cell, also known as the proton pump.

Administer with the first meal of the day; children with nasogastric or gastrostomy tubes may have granules mixed with an acidic juice, and then the tubes are flushed to prevent blockage.

Omeprazole (Prilosec)

Inhibits gastric acid secretion. Used for the short-term treatment (4-8 wk) of GER disease.

Esomeprazole (Nexium, Nexium 24HR)

S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells. Used in severe cases and in patients not responding to H2 antagonist therapy. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers; may be used up to 8 wk to treat all grades of erosive esophagitis.

Lansoprazole (Prevacid, Prevacid Solu Tab, Prevacid 24HR)

Suppresses gastric acid secretion by specific inhibition of the (H+, K+)-ATPase enzyme system (ie, proton pump) at the secretory surface of the gastric parietal cell. It blocks the final step of acid production. The effect is dose-related and inhibits both basal and stimulated gastric acid secretion, thus increasing gastric pH.