Aspiration Syndromes Clinical Presentation

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]

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, spitting, or vomiting
  • Apnea, bradycardia, cyanotic episodes
  • 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)
  • ALTE
  • Hiccups
  • Recurrent episodes of pneumonia or bronchitis
  • Cystic fibrosis
  • Bronchopulmonary dysplasia
  • Pulmonary abscess
  • Pulmonary fibrosis
  • Bronchiectasis
  • Chronic bronchitis
  • Obliterative bronchiolitis
  • Other chronic lung diseases

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

• 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.^[15] 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.