Aspiration

Kimberly A. Robinson

Richard S. Irwin

Aspiration is defined in Webster’s New Universal Unabridged Dictionary as inhaling fluid or a foreign body into the bronchi and lungs [1]. The foreign material may be particulate matter, irritating fluids (e.g., HCl, mineral oil, animal fat), or oropharyngeal secretions containing infectious agents. Although infectious pneumonias can be caused by inhaling air-containing organisms (e.g., infectious aerosols), aspiration of oropharyngeal contents or regurgitated gastric material is the primary manner in which bacterial pathogens are introduced into the lower respiratory tract. In fact, studies indicate that 5% to 15% of cases of community-acquired pneumonia are aspiration pneumonia [2]. The medical literature is not as precise, however, in defining aspiration-induced pulmonary injury or diagnosing its occurrence. For instance, the term aspiration pneumonia strongly denotes infectious sequelae to the aspiration event. However, there is a wide spectrum of conditions that result from aspirating foreign matter with varying clinical courses, not all of which are caused by infection [3,4,5]. It is difficult to predict exactly which course a patient will follow after an event. Although aspiration of a large volume of sterile gastric contents will likely lead to a chemical pneumonitis, aspiration of contaminated gastric contents will more likely
result in an infectious pneumonia. Although the frequency of all clinically significant aspirations in the intensive care unit (ICU) setting is not known, a review of Table 54.1 suggests that aspiration syndromes are common causes of pulmonary disease in the critically ill patient. An in-depth discussion of drowning can be found in Chapter 54.

Table 54.1 Aspiration Syndromes

Mendelson syndrome
Foreign body aspiration
Bacterial pneumonia and lung abscess
Chemical pneumonitis
Exogenous lipoid pneumonia
Recurrent pneumonias
Chronic interstitial fibrosis
Bronchiectasis
Mycobacterium fortuitum or chelonei pneumonia
Diffuse aspiration bronchiolitis
Tracheobronchitis
Tracheoesophageal fistula
Chronic persistent cough
Bronchorrhea
Drowning

Normal Defenses Against Aspiration and the Manner in Which They May Fail

Pathogenesis

Syndromes caused by aspiration are determined by (a) the material aspirated, (b) the amount aspirated, and (c) the state of the patient’s defenses at the time of the event. An understanding of the normal defenses and how and when they become impaired is also the cornerstone for an understanding of the pathogenesis of the various aspiration syndromes.

Because gastric acid prevents bacterial growth, the gastric contents are sterile under normal conditions [6]. Nevertheless, it has long been thought that the pH of aspirated contents determined the clinical course, with lower pH aspirates portending a worse outcome. Elevation of gastric pH to protect the lung was cited as one reason to use prophylactic antacids in the critically ill patient. However, colonization of the stomach by pathogenic organisms may occur when the gastric pH is artificially elevated [7,8]. Therefore, routine intratracheal instillation of prophylactic antacids to minimize aspiration-related lung injury is not recommended. There is conflicting data as to whether or not proton pump inhibitors and H2 blockers increase the risk of pneumonia [9,10]. Continued use of prophylactic acid suppression to prevent gastric bleeding and ulceration is another issue entirely and is discussed in Chapter 92.

Upper Gastrointestinal Defenses

Gastrointestinal mechanisms normally work in a coordinated, synchronized fashion. The teeth break up large food particles, and the tongue propels fluid and masticated food into the hypopharynx. As the hypopharyngeal muscles prepare to move food into the esophagus, the epiglottis covers the laryngeal inlet and the vocal cords close and the upper esophageal sphincter (cricopharyngeus muscle) relaxes. Pharyngeal swallowing initiates primary peristaltic waves in the esophagus that carry fluid and food through a relaxed lower esophageal sphincter (LES) into the stomach. After the bolus enters the stomach, the LES then contracts and prevents, although not entirely, gastroesophageal reflux (GER).

Even in the absence of known trauma or neurologic insult that could affect the swallowing cascade, some of the previously mentioned defenses may become impaired with increasing age or during sleep leading to silent aspiration. The vocal cords close much more slowly after the age of 50 years and may not close at all during sleep or with sedation irrespective of age. Furthermore, the cough response to airway irritation is also decreased during sleep compared with the waking state and may be totally absent during rapid eye movement sleep. In fact, it has been estimated that half of all healthy adults aspirate oropharyngeal secretions during sleep [3].

The risk of aspirating fluid and food is increased when the normal swallowing and upper gastrointestinal mechanisms fail to work in a coordinated, synchronized manner. Failure to adequately masticate one’s food, such as in the edentulous or sedated patient, establishes a high risk for aspiration [11]. Aspiration also may occur when the bolus cannot readily be cleared from the pharynx owing to neuromuscular disorders of any cause [12,13,14,15]. Structural abnormalities like Zenker’s diverticulum places a patient at risk of aspiration because the diverticulum may empty “late” after the swallowing effort is completed, at the time when the vocal cords are abducted. Conditions in which vocal cord closure becomes excessively delayed (e.g., old age, debilitation, sedation, the presence of a tracheostomy, and after endotracheal extubation) place patients at high risk for aspiration.

Regurgitation and subsequent aspiration of stomach contents also occur in elderly, sedated, or sleeping patients, especially when their upper esophageal sphincter and LES have been rendered incompetent by an oral or nasogastric tube [16,17]. The risk of aspiration is enhanced when such a patient remains in the supine position [18], a scenario often encountered in the ICU setting.

Respiratory Defenses

For infectious agents to enter the lower respiratory tract (e.g., below the vocal cords), they must first escape aerodynamic filtration in the nose, mouth, and larynx. Particles larger than 10 μm in diameter never reach the lower respiratory tract because they are filtered out of the airstream in the upper airway. Particles between 2 and 10 μm in diameter can reach the airways, and those between 0.5 and 1.5 μm in diameter can reach the alveoli. This is particularly relevant as most bacteria are within this size range. Although mucociliary clearance removes the larger particles [19] from the larger airways, additional defense mechanisms are needed to clear the smaller particles. This is accomplished in respiratory bronchioles and alveoli primarily by the alveolar macrophages, aided by neutrophils [20]. Infectious agents are detoxified by lysozymes as part of the cellular clearance mechanism [21]. Enzymes secreted by alveolar macrophages, neutrophils, and proteases in mucus also contribute to the detoxification process.

The first line of defense is mucociliary clearance. The respiratory filtration system and mucociliary clearance may become overwhelmed with large-volume fluid and food aspiration or with large amounts of inhaled infectious agents. Respiratory defenses may also become ineffective in the following settings: inhalational or systemic general anesthesia, endotracheal intubation, endotracheal suctioning, hypercapnia and hyperoxia, smoking, asthma, chronic bronchitis, cystic fibrosis and bronchiectasis, and respiratory infections with viruses and Mycoplasma pneumoniae.

In the absence of mucociliary clearance, the airways can still be cleared of excessive secretions and foreign bodies if the patient has an effective cough [19]. However, cough is not a primary defense mechanism and only provides clearance when mucociliary clearance is inefficient or overwhelmed. An effective cough and rapid closure of the vocal cords might also limit the consequences of GER of gastric contents to a chemical laryngitis. Alternatively, an effective cough with slow closure of the vocal cords might limit the inhalational injury to a chemical tracheobronchitis. An effective cough is determined both by good expiratory flow rates and respiratory muscle strength [22]. Thus, cough may be ineffective in patients with severe asthma, chronic obstructive pulmonary disease, respiratory neuromuscular disorders, painful incisions, or in those receiving excessive sedation and analgesia with antitussive effects.

When the mechanical defenses are overwhelmed, alveolar macrophages represent the initial phagocytic response. These cells also trigger additional inflammatory and immune responses by secreting cytokines. This response is followed by the influx of neutrophils into the alveolar spaces. Neutrophils are critical for the eradication of bacterial agents and therefore any impairment in their function would be detrimental [20]. Aspirated bacteria cause infectious pneumonia when the alveolar phagocytes become impaired, such as in alcoholism, pH less than 7.2, acute alveolar hypoxia, alveolar hyperoxia, corticosteroid therapy, respiratory viral infections, hypothermia, starvation, and exposures to nitrogen dioxide, sulfur dioxide, ozone, and cigarette smoking on a long-term basis [3].

Immunologic defenses such as complement and immunoglobulins augment the nonimmunologic mechanisms previously mentioned by opsonizing bacteria for the alveolar phagocytes [23,24]. Although the role of immunologic defenses against infectious particles is sketchy, it is believed that they are important in augmenting and occasionally directing the alveolar phagocytes. For instance, patients with hereditary and acquired immunologic abnormalities, such as immunoglobulin G and complement deficiencies, are susceptible to frequent and often severe bacterial pneumonias. For a more complete list of references for this section, please refer to the previous edition of this chapter published in Irwin and Rippe’s Intensive Care Medicine, sixth Edition [3].

Prevalence of Aspiration in the Critically Ill

Aspiration should be considered in all ICU patients with a pulmonary problem. This is especially true for the elderly, debilitated, or sedated patient with unexplained deterioration in pulmonary status. Oral or nasal enteral feeding tubes that compromise the LES, anticholinergics that decrease gastric motility, history of dysphagia, and neck hyperextension increase the probability. The presence of an endotracheal tube or tracheostomy tube poses a high risk for aspiration and its consequences.

Translaryngeal Intubation

Clearly, no one to feed a patient with an oral or nasal endotracheal tube in place, given the obvious mechanical barrier and distortion of the swallowing structures. What is often less intuitive is that dysphagia may persist for a variable time after the endotracheal tube has been removed. It has been suggested that the swallowing reflex can be impaired for up to 48 hours after short-term extubation, but gradually improves within a week [25]. Recent data suggest that the addition of routine flexible endoscopic evaluation of swallowing (FEES) aids in the identification of patients who are at high risk of aspirating after endotracheal intubation [26,27,28,29]. Awake, postsurgical patients who were intubated for less than 28 hours for coronary artery bypass were evaluated for aspiration. Of the 24 patients examined immediately after extubation, 50% aspirated, whereas 25% and 5% aspirated when tested 4 and 8 hours, respectively, after extubation. Patients who were intubated for a longer duration of, on average, 6.3 ± 3.1 days also demonstrated a high incidence of aspiration when evaluated 2 to 3 days after extubation [30]. Twelve of the 22 patients aspirated when evaluated by modified barium swallow/video fluoroscopy (MBS/VF).

The basis of aspiration in patients who had translaryngeal intubation can be partially explained by well-documented changes of laryngeal and pharyngeal structure and function after extubation. Impaired laryngeal elevation, penetration, and pooling in the valleculae and pyriform sinuses can be witnessed on MBS/VF. Direct laryngoscopy revealed varying degrees of laryngeal edema in 94% of patients, in which 64% took up to 4 weeks to resolve [31]. Edema of the arytenoids, inflammation of the posterior aryepiglottic folds, and false vocal cords have also been described when evaluated 24 hours after decannulation [3]. Should aspiration occur, ciliary clearance and other respiratory defenses might not respond appropriately due to the physical insult of the endotracheal tube.

Tracheostomy Intubation

Patients with a tracheostomy tube, with or without dependence on mechanical ventilation, are also at high risk for aspiration. The tracheostomy tube interferes with proper laryngeal elevation that is necessary for effective glottic closure during swallowing [32], and an inflated cuff can compress neighboring swallowing structures, most notably the esophagus. Bronchoscopic evaluation of patients with chronic tracheostomy tubes often reveals laryngeal, pharyngeal, and subglottic edema, presumably owing to the irritation of pooled secretions. These anatomic changes may exacerbate dysphagia. In one study, despite a normal clinical bedside evaluation, a high clinical suspicion for aspiration prompted an MBS/VF examination, in which 63% of a selected group silently aspirated [33]. Another study evaluating the outcome of an MBS/VF examination of patients with chronic tracheostomies discovered that 50% aspirated, and 77% of the aspiration events were silent. These studies stress that bedside evaluation alone is insufficient to diagnose aspiration in these high-risk patients.

Enteral Feeding Catheters

Many patients in an ICU have nasal or oral gastric tubes for nutritional support. The mere presence of an oro- or nasogastric feeding tube increases the risk of reflux and aspiration by compromising the integrity and proper functioning of the LES by two mechanisms. First, the catheter prevents closure of the sphincter by direct mechanical interference. Second, the irritation of the pharynx by the tube promotes LES relaxation through vagally mediated pharyngeal mechanoreceptors [34]. In addition, the presence of a nasogastric feeding tube is associated with Gram-negative bacterial contamination of the oropharynx, which, when aspirated, can result in severe clinical deterioration [35].

Varying the size of the enteral feeding catheters and adjusting the location of the distal tip have been used in an attempt to minimize aspiration. However, decreasing the size of a nasal or oral tube for enteral feeding does not reduce GER or microaspiration events [36]. Small-bore feeding tubes appear to provide no added benefit with respect to reflux events, even when advanced to the postpylorus position [17,37]. Patients
with long-standing swallowing defects or on prolonged mechanical ventilation may be candidates for percutaneous gastrostomy or jejunostomy tubes; however, even percutaneous enteral feeding tubes alter lower esophageal tone and allow for reflux [38]. This manner of enteral feeding is not completely protective against aspiration despite bypassing the LES. In fact, patients fed by gastrostomy tubes have the same incidence of pneumonia as those fed by nasogastric tubes [39,40]. However, early gastrostomy may reduce the frequency of ventilator-associated pneumonia as compared with nasogastric tubes in stroke or head injury patients [41]. Feeding tubes offer no protection against colonized oral secretion or aspiration of gastric contents that, in the presence of tube feeds, have an increased pH and are often colonized with bacteria. Furthermore, although a percutaneous jejunostomy tube may minimize the large-volume aspiration events, it is a misconception that it prevents aspiration or decreases its incidence relative to a percutaneous gastrostomy tube [42].

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