Page of

Aspiration of gastric contents in the critically ill 

Aspiration of gastric contents in the critically ill
Aspiration of gastric contents in the critically ill
Oxford Textbook of Critical Care (2 ed.)

Sara Froio

and Franco Valenza


Key points

  • Several pulmonary syndromes may occur after aspiration, depending on the amount and nature of the aspirated material, the frequency of aspiration, and the host’s response to the aspirated material.

  • Aspiration of gastric contents results in a chemical burn of the tracheobronchial tree and pulmonary parenchyma, causing pneumonitis.

  • Aspiration pneumonia may involve fluid or particulate matter, which are not inherently toxic to the lung, but can cause airway obstruction or reflux airway closure.

  • The causative micro-organism in aspiration pneumonia, similar to community-acquired pneumonia, are thought to be bacteria residing in the oral cavity. In the treatment of aspiration pneumonia, use of antimicrobials for pneumonia itself is important.

  • The aspiration of gastric contents is generally preventable by good anaesthetic practice and attention to details in the intensive care unit.


Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower respiratory tract. Several pulmonary syndromes may occur after aspiration, depending on the amount and nature of the aspirated material, the frequency of aspiration, and the host’s response to the aspirated material. Aspiration pneumonitis is a chemical injury caused by the inhalation of sterile gastric contents, whereas aspiration pneumonia is an infectious process caused by the inhalation of oropharyngeal secretions that are colonized by pathogenic bacteria. Other aspiration syndromes include airway obstruction, lung abscess, exogenous lipoid pneumonia, and chronic interstitial fibrosis [1,2].

The three syndromes that are most frequently seen clinically and are best studied are chemical pneumonitis, bacterial infection, and airway obstruction. Although there is some overlap among these syndromes, they are distinct clinical entities. This chapter focuses on the pathophysiology, clinical features, and management of these three syndromes (Table 106.1).

Table 106.1 Classification of aspiration syndromes


Pulmonary sequelae

Clinical features

Management features

Aspiration pneumonitis

Chemical injury

  • Dyspnoea, tachycardia

  • Hypoxaemia

  • Tracheal suction

  • Antibiotics for superimposed infection

Aspiration pneumonia

Bacterial infection

  • Usually insidious onset

  • Cough, fever, purulent sputum

  • Radiograph: infiltrate involving dependent pulmonary segment or lobe


Airways obstruction

Mechanical obstruction

  • Dependent upon level of obstruction:

    • Acute dyspnoea

    • Cyanosis

    • Apnoea

  • Pulmonary oedema

  • Tracheal suction

  • Extraction of particulate matter

The lack of specific and sensitive markers of aspiration complicates the epidemiological study of aspiration syndromes. Furthermore, most studies do not distinguish between aspiration pneumonitis and aspiration pneumonia.

The risk of aspiration pneumonitis is approximately 10% after a drug overdose. This condition is very common in patients with reduced consciousness level due to general anaesthesia, particularly during pregnancy, where there is increased intra-abdominal pressure and delayed gastric emptying. The most recent report suggests an incidence of 1 in 3000 patients receiving general anaesthesia. However, mortality remains very high and accounts for 10–30% of all deaths related to anaesthesia. The elderly, particularly the nursing home population, is at increased risk of aspiration secondary to both an increased incidence of pharyngeal dysmotility and gastro-oesophageal reflux. Aspiration pneumonia and pneumonitis are the most common causes of death in patients with dysphagia caused by neurological disorders [1]‌.

Conditions that predispose to aspiration of gastric content include:

  • Reduced consciousness resulting in a compromise of the cough reflex and glottic closure.

  • Neurological dysphagia.

  • Disorders of the upper gastrointestinal (GI) tract, including oesophageal disease, surgery involving the upper airways or oesophagus, and gastric reflux.

  • Disruption of the gastro-oesophageal junction due to tracheostomy, endotracheal intubation, bronchoscopy, upper endoscopy, and nasogastric feeding.

  • General anaesthesia.

  • Extremes of age.

Clinical syndromes

Aspiration pneumonitis


The term aspiration pneumonitis refers to the aspiration of substances that are toxic to the lower airways, independent of bacterial infection. Gastric acid is the most frequently encountered and the most completely studied substance that can initiate an inflammatory reaction. Historically, the syndrome most commonly described as aspiration pneumonitis is Mendelson’s syndrome, reported in 1946 in patients who aspirated while receiving general anaesthesia during obstetrical procedures. Mendelson revealed the importance of acid in the pathogenesis of this syndrome when he showed that acid gastric contents introduced into the lungs of rabbits caused severe pneumonitis that was indistinguishable from that caused by an equal amount of 0.1 N hydrochloric acid. Later, it was shown that if the pH of gastric contents was neutralized before aspiration, the pulmonary injury was minimal. In experimental studies, the severity of lung injury increased significantly as the volume of the aspirate increases and as its pH decreases [3,4].

The pathophysiology of acid pneumonitis has been studied in experimental animals by intratracheal inoculation of sterile hydrochloric acid. These animal models require an inoculum that has a pH of ≤2.5 and that is relatively large (usually 1–4 mL/kg). This would translate to an inoculum of at least 25 mL of gastric acid in adult humans. It is probable that smaller volumes produce a more subtle process that either escapes clinical detection or causes a less fulminant form of pneumonitis. The clinical observation that patients with oesophageal or gastric reflux experience frequent bouts of recurrent pneumonitis, often accompanied by pulmonary fibrosis, supports this concept [5,6,7].

Aspiration of gastric contents results in a chemical burn of the tracheobronchial tree and pulmonary parenchyma, causing an intense parenchymal inflammatory reaction. Experimental animal studies have shown that the toxic effects of acid are immediate and extensive. Within 3 minutes there is atelectasis, due to acid denaturation of surfactant, peribronchial haemorrhage, pulmonary oedema, and degeneration of bronchial epithelial cells [8]‌.

By 4 hours, the alveolar spaces are filled with polymorphonuclear leucocytes and fibrin. Hyaline membranes are seen within 48 hours. The lung at this time is also grossly oedematous, haemorrhagic, and with alveolar consolidation.

At first, the caustic effects of the low pH of the aspirate are directed to the cells lining the alveolar–capillary interface—a second phase is associated with the infiltration of neutrophils into the alveoli and lung interstitium, with histological findings characteristics of acute inflammation. The mechanisms of the lung injury after gastric aspiration involve the release of pro-inflammatory cytokines, especially tumour necrosis factor-alpha (TNFα‎) and interleukin IL-8. In animal studies, neutropenia, inhibition of neutrophil function, inactivation of IL-8, and complement inactivation attenuate the acute lung injury induced by acid aspiration.

Under normal condition the gastric contents are sterile because of acidity. Bacterial infection does not have an important role in the early stages after the aspiration of gastric contents, but it may occur at later stages. Colonization of gastric contents may occur when the pH in the stomach is increased by the use of antacids. In addition, there may be gastric colonization by Gram-negative bacteria in patients who receive enteral feeds, as well as in patients with gastroparesis or small bowel syndrome [9,10].

Clinical features and diagnosis

The diagnosis of acid pneumonitis is usually presumptive.

The following clinical features should raise the possibility of chemical pneumonitis:

  • Abrupt onset of symptoms with prominent dyspnoea.

  • Fever that is usually low grade.

  • Cyanosis and diffuse crackles on lung auscultation.

  • Severe hypoxaemia and infiltrates on chest radiograph involving dependent pulmonary segments.

The dependent lobes in the upright position are the lower lobes. However, aspiration that occurs while patients are in the recumbent positions may result in pneumonia in the superior segments of the lower lobes and the posterior segments of the upper lobes. After a suspected aspiration, chest X-ray abnormalities typically appear within 2 hours. If performed, bronchoscopy demonstrates erythema of the bronchi, indicating acid injury.

The course of the disease varies. In one retrospective review of 50 cases, three outcomes were observed:

  • 12% of patients had a fulminant course and died shortly after aspiration presumably from acute respiratory distress syndrome (ARDS).

  • 62% had a rapid clinical improvement with clearing of the chest radiograph.

  • 26% had initial rapid improvement, but then developed new expanding infiltrates on chest X-ray, which probably represented secondary bacterial infection or the development of ARDS superimposed on the acid injury [11].


Patients with an observed aspiration should be placed in the head-down position on the right side and should have also immediate tracheal suction to maintain a clear airway. However, this manoeuvre will not protect the lungs from chemical injury, which occurs instantly in a manner that has been compared with a ‘flash burn’. The acid inoculum is rapidly neutralized by the physiological response. Pulmonary lavage is futile, since the full extent of injury has usually occurred by the time the diagnosis is recognized.

The major therapeutic approach is to correct hypoxia and support pulmonary function by assisted ventilation or positive-pressure oxygen. Endotracheal intubation should be considered for patients who are unable to protect their airways.

The use of corticosteroids in the treatment of chemical pneumonitis is controversial. Studies in animals have failed to demonstrate beneficial effects of corticosteroids on pulmonary function, lung injury, alveolar–capillary permeability, or outcome after acid aspiration. Furthermore, given the failure of two multicentre, randomized controlled trials to demonstrate a benefit of high-dose corticosteroids in patients with ARDS, the administration of corticosteroids cannot be recommended [12,13,14].

Although it is common practice, the prophylactic use of antibiotics in patients in whom aspiration is suspected or witnessed is not recommended. Similarly, the use of antibiotics shortly after aspiration in patients in whom a fever, leukocytosis, or a pulmonary infiltrate develops is discouraged, since the antibiotic may select for more resistant organisms in patients with an uncomplicated chemical pneumonitis. However, empirical antibiotic therapy is appropriate for patients who aspirate gastric contents, and who have small-bowel obstruction or other conditions associated with colonization of the gastric contents. Antibiotic therapy should be considered for patients with aspiration pneumonitis that fails to resolve within 48 hours following aspiration. Empirical therapy with broad-spectrum agents is recommended; antibiotics with anaerobic activity are not routinely required. Sampling of the lower respiratory tract (with a protected specimen brush or by broncho-alveolar lavage) and quantitative culture in intubated patients may allow targeted antibiotic therapy, or in patients with negative cultures, the discontinuation of antibiotics.

Aspiration pneumonia


Aspiration pneumonia develops after the inhalation of colonized oropharyngeal material. Aspiration of colonized secretions from the oropharynx is the primary mechanism by which bacteria gain entrance to the lungs. The causative micro-organism in aspiration pneumonia, similar to community-acquired pneumonia, are thought to be bacteria residing in the oral cavity. In fact, the risk of aspiration pneumonia is lower in patients without teeth and in patients who receive aggressive oral care.

Any condition that increases the volume or the bacterial burden of oropharyngeal secretions in a person with impaired defence mechanisms may lead to aspiration pneumonia.

This condition is generally less fulminant than acid pneumonitis and the actual episode of aspiration is seldom observed.

Clinical features and diagnosis

In patients with aspiration pneumonia, unlike those with aspiration pneumonitis, the episode of aspiration is frequently not witnessed and the diagnosis is often inferred when a patient at risk of aspiration has radiographic evidence of an infiltrate in characteristic bronchopulmonary segment. The presenting findings in aspiration pneumonia due to bacterial infection are variable depending on the time when the patient is seen during the course of the infection, the bacterial agents involved, and the status of the host.

Compared with most cases of community-acquired pneumonia, the course of the disease in this type of aspiration pneumonia often evolves slowly. The majority of patients presents with the common manifestations of pneumonia, including cough, fever, purulent sputum and dyspnoea, but the process evolves over a period of days or weeks instead of hours. If not treated, these patients have a high incidence of cavitation and abscess formation in the lungs in later stages [15].

Organisms that assume the greatest importance in terms of pathogenetic potential are anaerobic bacteria. Expectorated sputum is unsuitable for anaerobic culture because of inevitable contamination by the normal flora of the mouth. There is a limited experience with quantitative cultures of specimens obtained at bronchoscopy by a protected brush or broncho-alveolar lavage. In current practice, anaerobic bacteria are virtually never detected in pulmonary infections due to the lack of access to specimens that are uncontaminated with the normal flora of the upper airways, such as needle aspirated, trans-tracheal aspirates and pleural fluid.

Most patients with aspiration pneumonia acquired in the community have infection of mixed agents (anaerobic and aerobic bacteria such as S. pneumoniae, S. aureus, H. influentiae, and Enterobacteriaceae). By contrast, patients with nosocomial aspiration pneumonia commonly involve a mixture of anaerobes and Gram-negative bacilli such as E. coli, Klebsiella, and Pseudomonas. One recent prospective study of 95 patients from a long-term care facility admitted to an intensive care unit with pneumonia and risk factors for aspiration found that Gram-negative bacilli were the most common isolates (49%) followed by anaerobes (16%) and S. aureus (12%) [16].

One explanation for the difference in organisms accompanying anaerobic bacteria in hospitalized patients is the high frequency of upper airway colonization by enteric Gram-negative bacilli.


In contrast to chemical pneumonitis, antibiotics are the most important component of treatment of aspiration pneumonia due to bacterial infection. The choice of antibiotics should depend on the setting in which the aspiration occurs, as well as the patient’s general health. Historically, the antibiotic of choice for the treatment of aspiration pneumonia and lung abscess involving anaerobic bacteria was penicillin, usually given intravenously or orally in high doses. However, a recent trial evaluated the efficacy of agent with specific anaerobic activity, such as clindamycin and metronidazole. Antibiotic agents with activity against Gram-negative organism, such as third-generation cephalosporins, fluoroquinolones, and piperacillin, are usually required.

When anaerobic bacteria are suspected, clindamycin (600 mg iv every 8 hours) is suggested as first line therapy. Alternative agents, as suggested by clinical trials, are amoxicillin-clavulanic acid (875 mg po bd) or the combination of metronidazole (500 mg po or endovenous tds) plus amoxicillin (500 mg po tds). For nosocomial aspiration pneumonia aerobic bacteria, especially Gram-negative bacilli and S. aureus, are usually more important than the anaerobes and therapy should be directed at these organisms [17].

The usual duration of therapy for cases that are not complicated by cavitation or empyema is 7–10 days. Patients with lung abscesses need a longer course of antibiotics, usually until there is radiographic clearance or significant improvement.

Airway obstruction


Aspiration pneumonia may involve fluid or particulate matter, which are not inherently toxic to the lung, but can cause airway obstruction or airway closure.

Typical fluids that are aspirated and are not toxic to the lungs per se, include saline, barium, ingested fluid (including water), and gastric contents with a pH exceeding 2.5. Aspiration of large volumes of non-toxic fluid produces abrupt suffocation by mechanical obstruction. Failure to clear the airways may be impaired in patients who lack an effective cough reflex due to a neurological deficit or coma [18].

Clinical features and diagnosis

Patients who have aspirated gastric material may present with dramatic signs and symptoms. In solid particle aspiration, the severity of respiratory obstruction depends on the relative size of the particle that is aspirated and the calibre of the lower airways. When smaller particulate reaches peripheral airways causing complete or partial obstruction, the initial symptom is cough due to bronchial irritation. Chest radiograph shows atelectasis or obstructive emphysema. When major bronchi are involved there may be severe dyspnoea, cyanosis, wheezing, chest pain, pulmonary oedema, hypotension, and hypoxaemia with rapid progression to severe ARDS and death.

Bacterial superinfection is a frequent complication when the obstruction persists for more than 1 week.


The obvious therapeutic modality for the aspiration of large volume of non-toxic fluids is immediate tracheal suction. In the absence of a residual pulmonary infiltrate, no further treatment is indicated.

The immediate suggested treatment when major bronchi are involved is the Heimlick manoeuvre to dislodge the particle. When the obstruction is only partial, the primary therapeutic modality is removal of the particles with fibre optic or rigid bronchoscopy.


The main aim of aspiration treatment is prevention. Patient at risk must be identified, including emergency cases, pregnant women, and diabetics. A good anaesthetic practice and attention to detail for patients in the intensive care unit (ICU) are required. Safe intubation needs to be fasted after a rapid sequence induction with correct use of cricoid pressure.

The accepted minimum time for solid food to be emptied from the stomach in adults is 6 hours. Other approaches to prevention include the use of awake intubation and the use of balloon-tipped nasogastric tubes to attempt to occlude the cardia. Another element in prevention is the prophylactic use of anti-acids. A number of agents given pre-operatively have been shown to both increase effectively the pH and to reduce the volume of gastric contents.

In the ICU, similar preventive measures should be applied for intubation of patients, many of whom will also have nasogastric tubes inserted. Even a tracheostomy does not completely eliminate the risk of aspiration.

Bacterial colonization of gastric contents and oropharyngeal secretions, with subsequent aspiration to the lower airways are the most commonly recognized pathogenic factors for the development of nosocomial pneumonia.

Safe extubation is also an important factor in ICU, where patients can have an endotracheal tube in position several days. Patients must be able to cough and have an adequate gag reflex, the stomach contents must be aspirated, and the patient should be placed in the sitting position.

It has been recently observed that both body position and the time the patient is kept in that position are factors that increase the risk of aspiration of gastric contents to lower airways, increasing the risk of nosocomial pneumonia development. This suggests that the semi-recumbent position could be a non-cost prophylactic measure for nosocomial pneumonia.

A number of research groups are studying factors that affect aspiration from the oropharynx into the lower airways in mechanically-ventilated patients as the type of endotracheal cuff, with low-volume high-pressure cuffs.

In ICU patients, once nasogastric feeding has commenced, preventing gastric dilatation by regular aspiration of gastric contents to determine effectiveness of gastric emptying is essential. In patients with gastroparesis leading to gastric distention and regurgitation, the use of post-pyloric tube for feeding may have advantages [19,20].

Measures that should be implemented to prevent silent aspiration include elevating the head (of the bed), oral care, and adequate nutrition to prevent muscle deterioration.


1. Marik PE. (2001). Aspiration pneumonia and aspiration pneumonitis New England Journal of Medicine, 344(9), 665.Find this resource:

2. Bartlett JG and Gorbach SL. (1975). The triple threat of aspiration pneumonia. Chest, 68, 560.Find this resource:

3. Mendelson CL. (1946). The aspiration of stomach contents into the lungs during obstetric anesthesia. American Journal of Obstetrics and Gynecology, 52, 191–205.Find this resource:

4. Tebeaut JR. (1952). Aspiration of gastric contents: an experimental study. American Journal of Pathology, 28, 51–67.Find this resource:

5. Fisk RL, Symes JF, Aldridge LL, and Couves CM. (1970). The pathophysiology and experimental therapy of acid pneumonitis in ex vivo lungs. Chest, 57, 364.Find this resource:

6. Mays EE, Dubois JJ, and Hamilton GB. (1972). Pulmonary fibrosis associated with tracheobronchial aspiration. A study of the frequency of hiatal hernia and gastroesophageal reflux in interstitial pulmonary fibrosis of obscure etiology. Chest, 69, 512.Find this resource:

7. Johnson LF and Rajagopal KR. (1988). Aspiration resulting from gastroesophageal reflux. A cause of chronic bronchopulmonary disease. Chest, 93, 676.Find this resource:

8. Davidson BA, Knight PL, Wand Z, et al. (2005). Surfactant alterations in acute inflammatory lung injury from aspiration of acid and gastric particulates. American Journal of Physiology - Lung Cellular and Molecular Physiology, 288, L699–708.Find this resource:

9. Garvey BM, McCambley JA, and Tuxen DV. (1989). Effects of gastric alkalinization on bacterial colonization in critically ill patients. Critical Care Medicine, 17: 211–16.Find this resource:

10. Bonten MJ, Gaillard CA, van der Geest S, et al. (1995). The role of intragastric acidity and stress ulcus prophylaxis on colonization and infection in mechanically ventilated ICU patients: a stratified, randomized, double-blind study of sucralfate versus antacids. American Journal of Respiratory and Critical Care Medicine, 152, 1825.Find this resource:

11. Bynum LJ and Pierce AK. (1976). Pulmonary aspiration of gastric content. American Reviews in Respiratory Diseases, 114, 1129.Find this resource:

12. Bernard GR, Luce JM, Sprung CL, et al. (1987). High-dose corticosteroides in patients with the adult respiratory distress syndrome. New England Journal of Medicine, 317, 1565.Find this resource:

13. Bone RC, Fisher CJ, Jr, Clemmer TP, Slotman GJ, and Metz CA. (1988). Early methylprednisolone treatment for septic syndrome and the adult respiratory distress syndrome. Chest, 94, 448.Find this resource:

14. Wynne JW, DeMarco FJ, and Hood CI. (1981). Physiological effects of corticosteroids in foodstuff aspiration. Archives of Surgery, 116, 46.Find this resource:

15. Bartlett JC. (1993). Anaerobic bacterial infections of the lung and pleural space. Clinical Infectious Diseases, 16(Suppl. 4), S248.Find this resource:

16. El-Solh AA, Pietrantoni C, Bhat A, et al. (2003). Microbiology of severe aspiration pneumonia in institutionalized elderly. American Journal of Respiratory and Critical Care Medicine, 167, 1650.Find this resource:

17. Kadowaki M, Demura Y, Mizuno S, et al. (2005). Reappraisal of clindamicyn IV monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly patients. Chest, 127, 1276.Find this resource:

18. Colebatch HJ and Halmagyi DF. (1964). Reflex airway reaction to fluid aspiration. Journal of Applied Physiology, 17, 787.Find this resource:

19. Bonten MJ, Gaillard CA, van der Hulst R, et al. (1996). Intermittent enteral feeding: the influence on respiratory and digestive tract colonization in mechanically ventilated intensive care unit patients. American Journal of Respiratory and Critical Care Medicine 154, 394.Find this resource:

20. Bonten MJ, Gaillard CA, van Tiel FH, van der Geest S, and Stobberingh EE. (1994). Continuous enteral feeding counteracts preventive measures for gastric colonization in intensive care unit patients. Critical Care Medicine, 22, 939.Find this resource:

Copyright © 2022. All rights reserved.