The inhalation of oropharyngeal or gastric contents into the respiratory tracts is called ‘pulmonary aspiration’. In 1946, Mendelson1 described for the first time 66 cases of pulmonary aspiration in obstetric anaesthesia patients in a New York hospital. This survey showed that aspiration of solid material produced bronchial obstruction, whereas aspiration of liquid material provoked an asthma-like syndrome. In the meantime, it became clear that aspiration can lead to a variety of disorders such as bronchitis, exacerbation of asthma, chemical pneumonitis, infectious pneumonia, acute lung injury or acute respiratory distress syndrome, and is, therefore, an important cause of serious illness.2 Although a strict definition is not possible, there are two categories of acid aspiration based on contrasting features: aspiration pneumonia and aspiration pneumonitis. Aspiration pneumonia is most often seen in elderly patients and is an unwitnessed event. Colonised oropharyngeal material, including Gram-negative, Gram-positive and anaerobic bacteria leads to an acute inflammatory process. Five to 15% of community-acquired pneumonias are aspiration pneumonia, mostly due to dysphagia and abnormal gastric motility.2,3 Patients present with tachypnoea, cough and, eventually, with signs of pneumonia. In contrast, in aspiration pneumonitis, which is most often a witnessed event, acidic and particulate gastric material induces an acute lung injury. A major predisposing factor is a depressed level of consciousness due to anaesthetic agents, drug overdose, seizures or cerebrovascular insults. Patients with an aspiration pneumonitis have either no symptoms or symptoms ranging from non-productive cough to respiratory distress. Aspiration pneumonitis can be a life-threatening condition.
This review article will mainly focus on aspiration pneumonitis as an intraoperative event.
The reported incidence of aspiration pneumonitis in the peri-operative setting varies in the literature, probably due to a lack of specific and sensitive markers. In addition, most studies do not distinguish between aspiration pneumonia and aspiration pneumonitis. Even without knowing the exact number of events, we can estimate that pulmonary aspiration is relatively infrequent. Several retrospective, as well as prospective, studies have been performed, suggesting an incidence between 2.9 and 4.7 aspirations per 10 000 general anaesthetics in a mixed population of adults and children.4 Warner et al.5 published data from a study of 215 488 anaesthetics and observed 67 episodes of aspiration in adults (3.1 per 10 000 patients) undergoing general anaesthesia. In 2006, a retrospective study was published focusing on the incidence and outcome of peri-operative pulmonary aspiration in non-obstetric adults at an American University Hospital over 4 years.6 With the help of two different databases, the authors tried to identify potential cases of peri-operative aspiration. They identified 14 cases out of 99 441 anaesthetics; half of these were observed during anaesthesia for gastrooesophageal procedures. Another study described the incidence of aspiration according to the surgical procedure.7 Tracheostomy surgery was associated with an incidence of aspiration of 19.1%, followed by interventions on the respiratory system at 2.1%, the nervous system and skin at 1.3 and 1.1%, respectively, and the digestive system at 1.1%.
Several studies have focused on children receiving general anaesthesia, wherein data regarding incidence of aspiration are contradictory. Whereas some studies suggest that children have a greater risk of pulmonary aspiration than adults,8,9 others have not confirmed this.10,11
A third group of aspiration events are those seen in obstetric patients. The incidence varies in this group in relation to the surgical procedure. One study reported an incidence of one in 6000 in obstetric patients receiving general anaesthesia for vaginal deliveries and one in 430 for caesarean section patients.12 In other studies, an aspiration incidence of one in 1547 and one in 1431, respectively, was described for caesarean section under general anaesthesia,13,14 and a recent audit showed an incidence of 1 in 900 in women undergoing caesarean section.15 The risk of pulmonary aspiration is, therefore, at least double or three times as high as in general surgical patients.16
In summary, the incidence of an aspiration event is infrequent in healthy adults without risk factors. A greater incidence is seen in paediatric and obstetric anaesthesia patients. It is not known whether the incidence has changed since the first description following changes to anaesthesia practice.
Aspiration of gastric acid induces a chemical burn triggering the release of various inflammatory mediators such as cytokines, chemokines and adhesion molecules that orchestrate the inflammatory response. All these inflammatory molecules serve as mediators to attract inflammatory effector cells such as neutrophils and alveolar macrophages and to activate leucocytes, further supporting the inflammatory cascade. In rats, a biphasic inflammatory pattern was observed with a first peak 1 h after injury and a second one after 4 h.17,18 These two peaks were reflected in the expression of nuclear factors and inflammatory mediators, as well as in the accumulation of neutrophils.18
The hypothesis that both the pH and the volume of gastric aspirate have crucial roles in determining the severity of lung injury has been increasingly challenged, both clinically and with respect to the immunopathological mechanisms.19,20 Studies on animals have indicated that pulmonary aspiration was self-limiting, even with aspirates of high volume or low pH.17,21–23 Aspiration injury models were established, using not only acidic liquid, but also non-acidified gastric particles and combinations of both acid and small food particles.24 Cell recruitment and expression of inflammatory mediators were most pronounced after injury with combined acid and small food particles, followed by non-acidified gastric particles and acid-induced injury.25 These data are supported by findings in patients wherein the most severe lung injury was observed in patients following aspiration with food particulate material.26,27
Morbidity and mortality
Morbidity can be determined by investigating the presence of pulmonary infiltrates, the use of antibiotics and bronchodilators and the duration of respiratory support. Such data are, however, rarely available. The reported mortality after aspiration varies. In an Australian survey, the mortality after aspiration was 3.5%,28 whereas it was 4.5% in a study at the Mayo Clinic.5 In obstetric anaesthesia, the mortality rate varies in a higher range of up to 12%. Although the number of anaesthetics for obstetric procedures has increased over recent decades, the death rate associated with aspiration has decreased as a result of the shift from general to regional anaesthesia for caesarean section.
According to the authors of a number of studies, emergency surgery (particularly, trauma and abdominal surgery with delayed gastric emptying) procedures performed at night and inadequate anaesthesia were associated with a higher incidence of pulmonary aspiration.5,8,28–30 In particular, aspiration is associated with manoeuvres to overcome a difficult intubation, during which anaesthesia can lighten and repetitive laryngoscopy can induce gagging and vomiting.5 Another important risk factor is patient age more than 60 years. Patients aged 80 years or over have an almost 10-fold increased risk of pulmonary aspiration compared with 20-year-olds.7 Aspiration occurs at various times in the peri-operative phase: the patient can vomit immediately before induction of anaesthesia, during laryngoscopy and at tracheal extubation.5
The two anatomical sites principally involved in preventing aspiration are the lower and upper oesophageal sphincters. Other crucial components determining the likelihood of aspiration are the gastric contents and the laryngeal reflexes. The risk factors for pulmonary aspiration resulting in pneumonia or aspiration pneumonitis are summarised in Table 1.
The lower oesophageal sphincter forms the border between the stomach and lower oesophagus. Decreased tone in the sphincter is considered responsible for gastrooesphageal reflux disease. Reflux is a common risk factor for aspiration. As shown in a recent study, 86% of healthy adult volunteers had abnormal laryngeal findings, which could be attributed to reflux.31 Laryngopharyngeal reflux is often, if not always, associated with bronchitis, presenting as a chronic cough or exacerbation of preexisting asthma. Forty-six percent of patients with severe asthma compared with 5% of controls have evidence of reflux on barium swallow.32 Apart from preexisting disease with impaired sphincter function, anaesthetic drugs such as volatile agents can decrease lower oesophageal pressure. Kohjitani et al.33 tested the effect of sevoflurane and enflurane on the lower oesophageal sphincter tone in children. Although both volatile anaesthetics had an inhibitory effect, the reduction was relatively small. Another study investigating the effect of the induction of anaesthesia with sevoflurane also showed a decrease of sphincter tone.34 In contrast with these findings with volatile anaesthetic agents, a study on pigs with full stomachs showed that rapid sequence induction with propofol and succinylcholine or thiopental and succinylcholine increased sphincter tone.35 The tone was enhanced before the onset of fasciculations and remained elevated during intubation. Whereas the non-depolarising muscle relaxant atracurium produced little change in sphincter tone, pancuronium increased it.36
Interestingly, drug effects on upper oesophagel sphincter tone are not always identical to the their actions on the lower sphincter. Although volatile anaesthetic agents have the same effect on the tone in the upper as in the lower sphincter,37 thiopental and succinylcholine lower the tone of the upper sphincter only.38 Atracurium results in a similar effect as on the lower sphincter.39 Taken together, the use of anaesthetic agents and muscle relaxants is likely to be associated with decreased sphincter tone and increased regurgitation. However, it is not clear whether changes in both the lower and upper oesophageal sphincter result in decreased barrier pressure and put the patient at increased risk of reflux-induced aspiration. The choice of technique for induction of anaesthesia might be more relevant in determining the risk of aspiration.
The severity of lung injury was thought to be associated with the volume and acidity of the aspirated material, its character (particulate matter or liquids), as well as the host response. For many years, it has been believed that patients would be at risk of aspiration pneumonitis if the volume of the gastric contents was 0.4 ml kg−1 and the pH less than 2.5. This assumption was based on a statement from an earlier study performed in obstetric anaesthesia patients.19 Some years after publication of this work, the authors revealed that they had drawn their conclusions from one experiment on one monkey, applying acid (0.4 ml kg) directly into the right main bronchus. The total gastric volume and pH do not necessarily represent the material that is aspirated. In addition, material with a higher pH seems to harm the lung. In dogs, aspiration of 2 ml kg−1 of gastric content with a pH of 5.9 induced a severe lung injury.40 Aspiration of bile with a pH of 7.19 caused extended aspiration pneumonitis in a porcine lung model.41
Critically ill surgical patients are at high risk of aspiration, especially after removal of the tracheal tube following a period of mechanical ventilation, due to the patient's supine position, gastroparesis and the presence of a nasogastric tube. Gastroparesis can result from the use of opioids (which increase gastric residual volume), after sepsis, extensive burns, trauma and surgery itself. Gastroenteral reflux seems to play an important role in these patients as well. Finally, many patients suffer from swallowing dysfunction after a period of intubation.
To prevent peri-operative aspiration, it is important to recognise patients at risk of aspiration (see Table 1). Fasting status and the choice of anaesthetic technique can play an important role.
The question of how long a patient should be ‘nil by mouth’ in various settings was addressed some years ago. The purpose of fasting is to minimise the volume of gastric contents. At the same time, thirst and dehydration should be avoided, and the duration of ‘nil by mouth’ should be limited to a minimum. Although it was thought that overnight fasting before anaesthesia would reduce acidity and the volume of the stomach contents, fasting policy has now changed to a more relaxed standard with new guidelines based on clinical trials.42,43 With the help of animal models, it has become clear that a gastric volume more than 0.4 ml kg−1 does not always lead to regurgitation and that fasting does not necessarily result in a low gastric volume. The minimum gastric volume required to produce regurgitation was determined in anaesthetised cats. A volume of 20.8 ml kg−1 was associated with gastric regurgitation and the risk of inducing aspiration pneumonitis.44 Studies on starved patients have shown gastric volumes exceeding 0.4 ml kg−1, but there was no evidence of aspiration.45,46
It has been suggested that clear liquids such as water, coffee without milk or fruit juice can be given to healthy patients for up to 2 h before the induction of anaesthesia. These guidelines are based on findings from Miller et al.43 who reported no difference in gastric volume in patients who were allowed to drink tea and eat toast up to 4 h before surgery compared with patients adopting a ‘nil by mouth’ after midnight regimen. Several subsequent studies have confirmed these findings in adults and children.42,47,48 For emergency procedures, the patient is at risk of pulmonary aspiration due to stress, pain, and the administration of opioids – all factors that slow down gastric emptying. These guidelines described above for elective patients cannot be applied to this population. In healthy patients, solids should be avoided after midnight; however, a light meal such as dry toast may be considered up to 6 h before anaesthesia.
Even though these standards are now established, they have been developed without any evidence from large, randomised, multicentre studies that have investigated post-operative complications in adults. A Cochrane review summarised the results of 22 studies, focusing on peri-operative complications in relation to a liberal fasting regimen with fluid intake such as water, coffee, fruit juice and clear fluids, compared with a strict ‘nil by mouth’ regimen.49 Most of the studies were performed in healthy adults without increased risk of regurgitation or aspiration. The volume or pH of gastric contents at the time of intubation did not significantly differ between groups with a shortened or standard fasting period. Patients with pre-operative water intake were found to have less volume of gastric contents with higher gastric pH values. There was no indication that the volume of fluid permitted during the pre-operative period resulted in a difference in outcome.
Pharmacological treatment to provide aspiration prophylaxis consists of several medication groups: antacids, these agents are most often given prior to induction of anaesthesia to neutralise rapidly the acidic pH of the stomach contents; H2-receptor antagonists and proton pump inhibitors, these drugs inhibit secretion of acid and reduce volume and acidity of the stomach contents; and prokinetic drugs, these are used to accelerate gastric emptying by increasing gastric motility. Reviewing the literature, it is clear that there are no data showing an improved outcome in healthy adults after the use of antacids, H2-receptor antagonists, proton pump inhibitors or prokinetics.16 In the absence of clear evidence, one has to consider that all these drugs can be associated with unwanted side-effects. The use of antacids increases gastric pH, but also increases gastric volume.50 It is not known whether aspiration of stomach contents, including antacids causes harm to the lung. Non-particulate antacids may be less likely to induce severe lung injury than particulate ones. H2-receptor antagonists have been associated with severe bradycardia or atrioventricular block, as well as hepatotoxicity and neurologic complications. Proton pump inhibitors can delay elimination of drugs such as diazepam or warfarin. The prokinetic metoclopramide can cause extrapyramidal disturbances. Finally, the financial impact of such therapies without any evidence of better outcome in the event of pulmonary aspiration must be borne in mind.
Several prospective randomised studies have investigated pretreatment of pregnant patients prior to the induction of anaesthesia. Treatment with antacids, H2-receptor antagonists, proton pump inhibitors, or a prokinetic prior to elective caesarean section was compared with placebo or no treatment in a Cochrane review.51 Twenty-two studies, involving 2658 women, were generally of poor quality and the information of limited value. The results were the same for all studies: antacids, H2-receptor antagonists and proton pump antagonists reduced the acidity of the stomach contents. Combined treatment with antacids and an H2-receptor antagonist may be the most efficient technique with a rapid reduction in the acidity with the use of antacids for intubation and the longer action of the H2-receptor antagonist for extubation. None of the studies, however, have focused on clinical outcome parameters.
Induction of general anaesthesia in patients at risk for pulmonary aspiration should be performed using a rapid sequence induction protocol. This technique is defined by several steps. The first step is preparation. The patient should be monitored and a safe intravenous access line established. There is no strict rule regarding the patient's position. Stept and Safar52 recommended the so-called ‘V position’ with the trunk elevated at 30° to counteract regurgitation and elevated feet to increase preload. Others argue for use of the Trendelenburg position53 or the supine position.54 A laryngoscope and a suction have to be ready for immediate use. The second step is preoxygenation. Thorough preoxygenation of the patient is a crucial part of rapid sequence induction, as it may avoid later desaturation during a possible difficult intubation. Patients particularly at risk of hypoxaemia during induction are the obese and obstetric patients as their functional residual capacity is decreased. The third step is premedication. Although opioids are not part of a traditional rapid sequence induction technique, their use has been investigated in several studies. Whereas some authors found that administering opioids resulted in a more stable haemodynamic profile,55 others have argued that respiratory drive is decreased if there is a failed intubation.56 Additionally, the possibility of rigidity is another argument against the use of opioids. The fourth step is application of neuromuscular blocking agents. Several studies have compared the effect of different induction agents in providing optimal intubation conditions and the least effect on haemodynamic stability. It is clear that propofol is superior to thiopental in suppressing pharyngeal and laryngeal reflexes.57 Etomidate is recommended when haemodynamics are impaired.58 Succinylcholine remains the cornerstone of rapid sequence induction.59 If there is a contraindication to succinylcholine, a non-depolarising muscle relaxant such as rocuronium can be used to facilitate intubation. The fifth step is prevention. In 1961, Sellick60 recommended applying cricoid pressure to prevent gastric insufflation and to increase pressure in the upper oesophageal sphincter. The question of whether cricoid pressure reduces the incidence of aspiration or mortality is not conclusively answered in the literature, however. Recommendations regarding the application of cricoid pressure are based on clinical observations and on data from animal and cadaver studies. Originally, a force of 44 N was suggested, starting while the patient is still conscious. More recently, recommendations have been changed to use of 10 N in the awake patient and 30 N after administration of induction agent.61 Several authors have claimed these forces are not used or are only used for a short time, which may explain the continuing cases of fatal aspiration despite the use of cricoid pressure.62,63 One other concern is that use of cricoid pressure may impair laryngeal visualisation during laryngoscopy.64
Considerable technical advances have been made in the last two decades in the development of new airway devices such as the laryngeal mask airway, the cuffed oropharyngeal airway, the oesophageal tracheal combitube and the laryngeal tube. When intubation has failed during a rapid sequence induction, the use of one of these devices may facilitate ventilation and prevent hypoxia, which, itself, can trigger aspiration.
Some patients may be at particular risk for intraoperative silent aspiration, even with a tracheal tube in place. The supine position with increased intraabdominal pressure as well as the frequent use of intraoperative transoesophageal echocardiography can lead to microaspirations, followed by post-operative pneumonia.65 Evaluating new cuff models is one target in preventing aspiration and requires further evaluation,66 but may be an important approach to decreasing the incidence of silent aspirations and associated post-operative pulmonary complications.
If pulmonary aspiration occurs during tracheal intubation, suctioning is indicated, followed by immediate orotracheal intubation.67 If particulate matter is aspirated, bronchoscopy should be performed and the particles removed. Further actions are dictated by subsequent findings; therapy is usually symptomatic; for example, bronchospasm is managed with bronchodilators. In general, treatment with antibiotics is not recommended as it may promote the growth of resistant organisms.68 Clinical outcome is not improved by a routine use of antibiotics in the acute phase of aspiration.69 However, if bowel contents are aspirated following an obstructive or paralytic ileus, antibiotics should be given. Targeted antibiotic therapy may be initiated after culture of bronchoalveolar lavage fluid. If aspiration pneumonitis has not resolved after 48 h and an organism has not yet been identified, penicillin and clindamycin are used as first-line antibiotics.70 Alternatively, a combination of a third-generation cephalosporin and clindamycin is used.
The beneficial effect of corticosteroids on lung function after acid aspiration with aspiration pneumonitis is still the subject of debate. The few existing studies reported no beneficial effect.67 Sukumaran et al.71 found patients given corticosteroids had a longer stay in the intensive care unit. Morbidity and mortality were the same for both corticosteroid and placebo group. Another study reported that patients treated with corticosteroids suffered more frequently with pneumonia due to Gram-negative bacteria.72
If an acute lung injury develops, a protective ventilatory strategy is required. A tidal volume of 6 ml kg−1 with a plateau pressure less than 30 cmH2O was shown to be successful in reducing mortality in the NIH Acute Respiratory Distress Syndrome Network study.73–75
Acid aspiration is an infrequent event in healthy surgical patients and the associated morbidity and mortality are low. However, the reported incidence and complication rates may be falsely low due to unwitnessed aspiration events. Prevention rules such as ‘nil by mouth’ and pharmacological treatment are based on routine practice and not on large clinical trials and are, therefore, of limited value. Most European countries adhere to pre-operative fasting guidelines of 2 h for clear fluids and 6 h for solids. Careful evaluation of the patient's risk profile and an anaesthesia plan chosen accordingly are important in avoiding an aspiration event. Known predisposing factors as well as emergency surgery imply a higher risk for the patient. Consideration of regional anaesthesia or, if necessary, general anaesthesia with a rapid sequence induction performed by an experienced anaesthesiologist under ideal conditions, may be crucial.
The authors declare no conflicts of interest or financial assistance.
1 Mendelson CL. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gyn 1946; 53:191–205.
2 Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001; 344:665–671.
3 Torres A, Serra-Batlles J, Ferrer A, et al
. Severe community-acquired pneumonia. Epidemiology and prognostic factors. Am Rev Respir Dis 1991; 144:312–318.
4 Ng A, Smith G. Gastroesophageal reflux and aspiration of gastric contents in anesthetic practice. Anesth Analg 2001; 93:494–513.
5 Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 1993; 78:56–62.
6 Sakai T, Planinsic RM, Quinlan JJ, et al
. The incidence and outcome of perioperative pulmonary aspiration in a university hospital: a 4-year retrospective analysis. Anesth Analg 2006; 103:941–947.
7 Kozlow JH, Berenholtz SM, Garrett E, et al
. Epidemiology and impact of aspiration pneumonia in patients undergoing surgery in Maryland, 1999–2000. Crit Care Med 2003; 31:1930–1937.
8 Olsson GU, Halken D, Hambraeus-Jonzon K. Aspiration during anaesthesia
: a computer-aided study of 185358 anesthetics. Acta Anaesthesiol Scand 1986; 30:84–92.
9 Murat I, Constant I, Maud'huy H. Perioperative anaesthetic morbidity in children: a database of 24 165 anaesthetics over a 30-month period. Pediatr Anesth 2004; 14:158–166.
10 Tiret L, Nivoche Y, Hatton F, et al
related to anaesthesia
in infants and children. A prospective survey of 40240 anaesthetics. Br J Anaesth 1988; 61:263–269.
11 Warner MA, Warner ME, Warner DO, et al
. Perioperative pulmonary aspiration in infants and children. Anesthesiology 1999; 90:66–71.
12 Krantz ML, Edwards WL. The incidence of nonfatal aspiration in obstetric patients. Anesthesiology 1973; 39:359.
13 Dindelli M, La Rosa M, Rossi R, et al
. Incidence and complications
of the aspiration of gastric contents syndrome during cesarean section in general anesthesia. Ann Ostet Ginecol Med Perinat 1991; 112:376–384.
14 La Rosa M, Piva L, Ravanelli A, et al
. Aspiration syndrome in cesarean section. Our experience from 1980 to 1990. Minerva Anestesiol 1992; 58:1213–1220.
15 Soreide E, Bjornestad E, Steen PA. An audit of perioperative aspiration pneumonitis in gynaecological and obstetric patients. Acta Anaesthesiol Scand 1996; 40:14–19.
16 Engelhardt T, Webster NR. Pulmonary aspiration of gastric contents in anaesthesia
. Br J Anaesth 1999; 83:453–460.
17 Kennedy TP, Johnson KJ, Kunkel RG, et al
. Acute acid aspiration lung injury in the rat: biphasic pathogenesis. Anesth Analg 1989; 69:87–92.
18 Madjdpour L, Kneller S, Booy C, et al
. Acid-induced lung injury: role of nuclear factor-kappaB. Anesthesiology 2003; 99:1323–1332.
19 Roberts RB, Shirley MA. Reducing the risk of acid aspiration during cesarean section. Anesth Analg 1974; 53:859–868.
20 James CF, Modell JH, Gibbs CP, et al
. Pulmonary aspiration: effects of volume and pH in the rat. Anesth Analg 1984; 63:665–668.
21 Goldman G, Welbourn R, Klausner JM, et al
. Attenuation of acid aspiration edema with phalloidin. Am J Physiol 1990; 259:L378–383.
22 Kudoh I, Ohtake M, Nishizawa H, et al
. The effect of pentoxifylline on acid-induced alveolar epithelial injury. Anesthesiology 1995; 82:531–541.
23 Knight PR, Kurek C, Davidson BA, et al
. Acid aspiration increases sensitivity to increased ambient oxygen concentrations. Am J Physiol Lung Cell Mol Physiol 2000; 278:L1240–1247.
24 Knight PR, Rutter T, Tait AR. Pathogenesis of gastric pariculate lung injury: a comparison and interaction with acid pneumonitis. Anesth Analg 1993; 77:754–760.
25 Knight PR, Davidson BA, Nader ND, et al
. Progressive, severe lung injury secondary to the interaction of insults in gastric aspiration. Exp Lung Res 2004; 30:535–557.
26 Pepe PE, Potkin RT, Reus DH, et al
. Clinical predictors of the adult respiratory distress syndrome. Am J Surg 1982; 144:124–130.
27 Fowler AA, Hamman RF, Good JT, et al
. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med 1983; 98:593–597.
28 Kluger MT, Short TG. Aspiration during anaesthesia
: a review of 133 cases from the Australian Anaesthetic Incident Monitoring Study (AIMS). Anaesthesia
29 Mellin-Olsen J, Fasting S, Gisvold SE. Routine preoperative gastric emptying is seldom indicated. A study of 85 594 anaesthetics with special focus on aspiration pneumonia. Acta Anaesthesiol Scand 1996; 40:1184–1188.
30 Borland LM, Sereika SM, Woelfel SK, et al
. Pulmonary aspiration in pediatric patients during general anesthesia: incidence and outcome. J Clin Anesth 1998; 10:95–102.
31 Hicks DM, Ours TM, Abelson TI, et al
. The prevalence of hypopharynx findings associated with gastroesophageal reflux in normal volunteers. J Voice 2002; 16:564–579.
32 Mays EE. Intrinsic asthma in adults. Association with gastroesophageal reflux. JAMA 1976; 236:2626–2628.
33 Kohjitani A, Shirakawa J, Satoh E, et al
. Effects of sevoflurane and enflurane on lower esophageal sphincter pressure and gastroesophageal pressure gradient in children. J Anesth 1999; 13:1–7.
34 Thorn K, Thorn SE, Wattwil M. The effects on the lower esophageal sphincter of sevoflurane induction and increased intra-abdominal pressure during laparoscopy. Acta Anaesthesiol Scand 2006; 50:978–981.
35 Tournadre JP, Barclay M, Bouletreau P, Chassard D. Lower oesophageal sphincter tone increases after induction of anaesthesia
in pigs with full stomach. Can J Anaesth 1998; 45:479–482.
36 Hunt PC, Cotton BR, Smith G. Comparison of the effects of pancuronium and atracurium on the lower esophageal sphincter. Anesth Analg 1984; 63:65–68.
37 Vanner RG, Pryle BJ, O'Dwyer JP, Reynolds F. Upper oesophageal sphincter pressure during inhalational anaesthesia
38 Vanner RG, Pryle BJ, O'Dwyer JP, Reynolds F. Upper oesophageal sphincter pressure and the intravenous induction of anaesthesia
39 McGrath JP, McCaul C, Byrne PJ, et al
. Upper oesophageal sphincter function during general anaesthesia
. Br J Surg 1996; 83:1276–1278.
40 Schwartz DJ, Wynne JW, Gibbs CP, et al
. The pulmonary consequences of aspiration of gastric contents at pH values greater than 2.5. Am Rev Respir Dis 1980; 121:119–126.
41 Porembka DT, Kier A, Sehlhorst S, et al
. The pathophysiologic changes following bile aspiration in a porcine lung model. Chest 1993; 104:919–924.
42 Kallar SK, Everett LL. Potential risks and preventive measures for pulmonary aspiration: new concepts in preoperative fasting guidelines. Anesth Analg 1993; 77:171–182.
43 Miller M, Wishart HY, Nimmo WS. Gastric contents at induction of anaesthesia
. Is a 4-h fast necessary? Br J Anaesth 1983; 55:1185–1188.
44 Plourde G, Hardy JF. Aspiration pneumonia: assessing the risk of regurgitation in the cat. Can Anaesth Soc J 1986; 33:345–348.
45 Ingebo KR, Rayhorn NJ, Hecht RM, et al
. Sedation in children: adequacy of two-hour fasting. J Pediatr 1997; 131:155–158.
46 Schwartz DA, Connelly NR, Theroux CA, et al
. Gastric contents in children presenting for upper endoscopy. Anesth Analg 1998; 87:757–760.
47 Splinter WM, Stewart JA, Muir JG. The effect of preoperative apple juice on gastric contents, thirst, and hunger in children. Can J Anaesth 1989; 36:55–58.
48 Schreiner MS, Triebwasser A, Keon TP. Ingestion of liquids compared with preoperative fasting in pediatric outpatients. Anesthesiology 1990; 72:593–597.
49 Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications
. Cochrane Database Syst Rev
50 Bond VK, Stoelting RK, Gupta CD. Pulmonary aspiration syndrome after inhalation of gastric fluid containing antacids. Anesthesiology 1979; 51:452–453.
51 Paranjothy S, Griffiths JD, Broughton HK, et al
. Interventions at caesarean section for reducing the risk of aspiration pneumonitis. Cochrane Database Syst Rev
52 Stept WJ, Safar P. Rapid induction-intubation for prevention of gastric-content aspiration. Anesth Analg 1970; 49:633–636.
53 Cameron JL, Zuidema GD. Aspiration pneumonia. Magnitude and frequency of the problem. JAMA 1972; 219:1194–1196.
54 Crawford JS. Anaesthesia
for caesarean section: a proposal for evaluation, with analysis of a method. Br J Anaesth 1962; 34:179–194.
55 Harris CE, Murray AM, Anderson JM, et al
. Effects of thiopentone, etomidate and propofol on the haemodynamic response to tracheal intubation. Anaesthesia
56 Richardson SP, Egan TD. The safety of remifentanil by bolus injection. Expert Opin Drug Saf 2005; 4:643–651.
57 Dobson AP, McCluskey A, Meakin G, Baker RD. Effective time to satisfactory intubation conditions after administration of rocuronium in adults. Comparison of propofol and thiopentone for rapid sequence induction of anaesthesia
58 Yeung JK, Zed PJ. A review of etomidate for rapid sequence intubation in the emergency department. CJEM 2002; 4:194–198.
59 Perry JJ, Lee JS, Sillberg VA, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev
60 Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia
. Lancet 1961; 2:404–406.
61 Vanner RG, Asai T. Safe use of cricoid pressure. Anaesthesia
62 Robinson JS, Thompson JM. Fatal aspiration (Mendelson's) syndrome despite antacids and cricoid pressure. Lancet 1979; 2:228–230.
63 Williamson R. Cricoid pressure. Can J Anaesth 1989; 36:601.
64 Haslam N, Parker L, Duggan JE. Effect of cricoid pressure on the view at laryngoscopy. Anaesthesia
65 Poelaert J, Depuydt P, De Wolf A, et al
. Polyurethane cuffed endotracheal tubes to prevent early postoperative pneumonia after cardiac surgery: a pilot study. J Thorac Cardiovasc Surg 2008; 135:771–776.
66 Dullenkopf A, Gerber A, Weiss M. Fluid leakage past tracheal tube cuffs: evaluation of the new Microcuff endotracheal tube. Intensive Care Med 2003; 29:1849–1853.
67 Janda M, Scheeren TW, Noldge-Schomburg GF. Management of pulmonary aspiration. Best Pract Res Clin Anaesthesiol 2006; 20:409–427.
68 Kalinowski CP, Kirsch JR. Strategies for prophylaxis and treatment for aspiration. Best Pract Res Clin Anaesthesiol 2004; 18:719–737.
69 Bynum LJ, Pierce LK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis 1976; 114:1129–1136.
70 Rebuck JA, Rasmussen JR, Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Crit Care Med 2001; 29:2239–2244.
71 Sukumaran M, Granada MJ, Berger HW, et al
. Evaluation of corticosteroid treatment in aspiration of gastric contents: a controlled clinical trial. Mt Sinai J Med 1980; 47:335–340.
72 Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med 1977; 63:719–722.
73 Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury
and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med
74 Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000; 342:1334–1349.
75 Fessler HE, Brower RG. Protocols for lung protective ventilation. Crit Care Med 2005; 33(Suppl):S223–S227.