Best Practice & Research Clinical Anaesthesiology Vol. 20, No. 3, pp.

409e427, 2006
doi:10.1016/j.bpa.2006.02.006 available online at http://www.sciencedirect.com

4 Management of pulmonary aspiration

Matthias Janda*
Consultant Anaesthetist
MD

Thomas W.L. Scheeren

Professor of Anaesthesiology

MD

ldge-Schomburg Gabriele F.E. No

Professor of Anaesthesiology and Chair

MD

Department of Anaesthesiology and Intensive Care Medicine, University of Rostock, Schillingallee 35, 18055 Rostock, Germany

Pulmonary aspiration of gastric contents in the perioperative phase is associated with increased postoperative morbidity and mortality. For the management of aspiration, differentiation between acid-associated aspiration pneumonitis and aspiration pneumonia as a consequence of a secondary bacterial contamination is of crucial importance. The incidence of aspiration in elective surgery is 1 per 2000e3000 anaesthesias in adults. In children, it is slightly more common with 1 per 1200e2600 anaesthesias. In the context of emergency anaesthesias the incidence of aspiration is three to four times higher. The risk particularly increases with recent ingestion of solid food or uids, with older patients, with pregnant women, and with consciousness-reduced patients. Besides giving a review of the pathophysiology, incidence, and the risk factors of aspiration, this article places emphasis on the practical management of this anaesthesia-associated complication. Cricoid pressure, as a non-evidence-based but clinically wide-spread method in the context of the prophylaxis of aspiration, is discussed critically. The main part deals with strategies to structure the management of aspiration by use of scientic concepts based on medical crisis management. For this, an algorithm based on current scientic investigations is presented. Key words: pulmonary aspiration; aspiration pneumonitis; aspiration pneumonia; cricoid pressure; rapid sequence induction; crisis management; treatment of aspiration.

* Corresponding author. Tel.: 49 381 494 6401; Fax: 49 381 494 6402. E-mail address: matthias.janda@medizin.uni-rostock.de (M. Janda). 1521-6896/$ - see front matter 2006 Elsevier Ltd. All rights reserved.

410 M. Janda et al

The aspiration of gastric contents is associated with a broad spectrum of possible clinical outcomes, ranging from mild asymptomatic and in themselves limited episodes of bronchial irritation up to the development of a severe pneumonitis with transition to an acute respiratory distress syndrome (ARDS).1 The pathogenesis of aspiration pneumonitis and aspiration pneumonia has been sufciently claried in the last few years, particularly in fundamental animal experiments. Surveys on the incidence and predisposing risk factors focused on particularly endangered patient collectives (emergency room admissions with higher ASA classication, pregnant women, patients with recent ingestion of solid food or uids, geriatric patients, and consciousness-reduced patients) and promoted the development of appropriate strategies for the prophylaxis of aspiration causing secondary morbidity and complications. Several randomized controlled studies in healthy adults undergoing elective surgery have reported that oral intake of clear uids up to 2 hr before anaesthesia induction occurs does not increase gastric uid volume or acidity.2 Thus, today the greatest value in the management of aspiration of gastric contents lies in the prevention of an aspiration. The treatment of pulmonary aspiration, however, is still limited primarily to a supporting therapy. Controlled studies of the gradual management of pulmonary aspiration do not yet exist. The use of evidence-based algorithms in the context of recognizing and treating aspiration could arrange the therapy more efciently and improve the patients outcome. PATHOPHYSIOLOGY Aspiration is dened as the entry of liquid or particulate matter into the tracheobronchial tree, as a consequence of passive regurgitation or active vomiting of gastric contents from patients without sufcient laryngeal protection reexes. Depending upon condition and composition of the aspirates, three different complications can be differentiated as a consequence of a pulmonary aspiration, without a strict demarcation in clinical practice: 1. acid-associated aspiration pneumonitis, 2. bacterial infection, 3. particle-associated aspiration. 1. Aspiration pneumonitis as a result of an acid-associated aspiration The classical aspiration pneumonia, the so-called Mendelson syndrome, was described by Mendelson in 1946 for the rst time.3 Here it concerns a chemical damage to the lung tissue due to the inhalation of sterile but very acid gastric contents. The extent of the lung tissue damage after aspiration of gastric secretion and/or contents occurring depends strongly on the pH value and on the quantity of the aspirate.4 However, the concept of critical borders described previously (pH value of the gastric juice < 2.5; volume > 0.4 ml/kg body weight or approximately 25 ml)5 has been questioned recently. Animal investigations have shown that rather the interrelationship of the factors pH value, volume, and presence of particles is of importance.6,7 Already small volumes can cause a high mortality rate if the pH value is very low. On the other hand, a higher volume can be tolerated if the gastric liquid

Management of pulmonary aspiration

411

is effectively buffered.8 Furthermore, in the pig model it was shown that the aspiration of bile acid with a pH of 7.19 leads to more serious physiological and histological changes of the lung than an aspiration of gastric acid with a pH of 2.24.9 The routine administration of drugs reducing gastric volume and acidity (antacids, H2-receptor blockers, proton pump inhibitors and prokinetic drugs) for acid aspiration prophylaxis has not been recommended by the ASA and should be considered in at-risk patients.10 Damage to the lung parenchyma after acid-associated aspiration typically proceeds in two phases.11 The rst phase is marked by a physiochemical process, which leads to direct toxic damage to the respiratory epithelium by the acid. Injury to the alveolo-capillary barrier with deletion of the type I-cells of the alveolar epithelium results in severe damage to the lung endothelium. An increased alveolar permeability leads to diffuse alveolar inltration with the development of an interstitial pulmonary edema. As a consequence, the lung compliance decreases and a mismatch of ventilation and perfusion occurs. The second phase, about 2 to 3 hr later, is dominated by immigration and activation of neutrophil granulocytes and presents an acute inammatory reaction. Inammatory cytokines play a central role as mediators for the lung parenchyma damage due to aspiration of acidic gastric contents. Interleukin-1b and tumor necrosis factor a are released by stimulated alveolar macrophages12 and stand as early response cytokines at the beginning of the inammatory cascade.6,13 They induce the production of further cytokines (e.g. IL-10) and chemokines (e.g. monocyte chemoattractant protein 1 [MCP-1], macrophage inammatory protein 1b [MIP-1b]), cytokine-induced neutrophil chemoattractant 1 [CINC-1], and macrophage inammatory protein 2 [MIP-2] by macrophages and mesenchymale cells.1,6,14 Neutrophils play a key role in the development of the lung injury also by the release of oxygen radicals and proteases.15,16 Clinically, aspiration pneumonitis can proceed both asymptomatically and in the range of a non-productive cough up to tachypnoea, bronchospasm, bloody cough, and the development of a respiratory insufciency 2 to 5 hr after the aspiration.17 2. Aspiration pneumonia as a consequence of a secondary bacterial infection Aspiration pneumonia is an infectious process, which is a consequence of the inhalation of oropharyngeal secretion or gastric contents contaminated with pathogenic bacteria. An acid-associated aspiration pneumonitis, on the other hand, favours the secondary development of aspiration pneumonia by superinfection with bacteria due to the destroyed respiratory epithelium.1,18 Although there is some overlap between aspiration pneumonitis and aspiration pneumonia, they are distinct clinical entities shown by Marik in Table 1.17 The composite of the aspirate depends on the germ spectrum in the particular hospital. Earlier studies of the germ spectrum of aspiration pneumonia identied anaerobic species as the typical pathogenic germs19e21, since these were isolated frequently from the oropharyngeal ora.22 Recent studies, however, have called into question the pathogenic role of aerobes in the context of aspiration pneumonia.23,24 Staphylococcus aureus (both methicilline sensitive and methicilline resistant), pseudomonas aeruginosa, enterobacter species, anaerobes, klebsiella species and escherichia coli rank among the most frequent pathogenic bacteria, without a dominance of an individual germ given.23,24 The aspiration event is often not observed. Especially in intensive care with longterm ventilatory support, silent aspiration occurs more frequently despite the use

412 M. Janda et al

Table 1. Contrasting features of aspiration pneumonitis and aspiration pneumonia (Copyright 2001 Massachusetts Medical Society17). Feature Mechanism Pathophysiologic process Bacteriologic ndings Chief predisposing factors Age group affected Aspiration event Typical presentation Aspiration pneumonitis Aspiration of sterile gastric contents Acute lung injury from acidic and particulate gastric material Initially sterile, with subsequent bacterial infection possible Markedly depressed level of consciousness Any age group, but usually young persons May be witnessed Patient with a history of a depressed level of consciousness in whom a pulmonary inltrate and respiratory symptoms develop No symptoms or symptoms ranging from a non-productive cough to tachypnoea, bronchospasm, bloody or frothy sputum, and respiratory distress 2 to 5 hr after aspiration Aspiration pneumonia Aspiration of colonized oropharyngeal material Acute pulmonary inammatory response to bacteria and bacterial products Gram-positive cocci, gram-negative rods, and (rarely) anaerobic bacteria Dysphagia and gastric dysmotility

Usually elderly persons Usually not witnessed Institutionalized patient with dysphagia in whom clinical features of pneumonia and an inltrate in a dependent bronchopulmonary segment develop Tachypnoea, cough, and signs of pneumonia

Clinical features

of cuffed tubes. Clinically, aspiration pneumonia is evidenced by coughs and tachypnea as well as typical symptoms of pneumonia, such as fever or shaking chills. The diagnosis is therefore inferred when a patient at risk of aspiration has radiographic evidence of an inltrate in a characteristic bronchopulmonary segment.17 3. Particle - associated aspiration Particle-associated aspiration is dened as the inhalation of particulate matter of gastric contents, resulting in an acute obstruction of smaller and possibly also larger airways with the consequence of sudden arterial hypoxemia and the development of atelectases distal to the foreign body. INCIDENCE AND RISK FACTORS The occurrence of pulmonary aspiration in the process of the patients perioperative care belongs to one of the most feared anaesthesia-associated incidents for most anaesthesiologists. According to Webb et al., aspiration and regurgitation are ranked the fth most common adverse event which can occur during general anaesthesia.25 The risk of aspiration has been examined in several studies in different countries in the past.26e36 However, the methodology of the individual studies is very different with partial retrospective, partial prospective designs. Secondly, the denitions for

Management of pulmonary aspiration

413

the inclusion of an event as perioperative pulmonary aspiration, the criteria of its diagnosis as well as the clear differentiation between aspiration pneumonitis and aspiration pneumonia vary between the individual studies. These factors make it hard to compare the results from these studies. Large studies on the incidence of aspiration and its associated mortality in the perianaesthetic period investigated in the last few decades are summarized in Table 2. Today the incidence of pulmonary aspiration in elective surgery is reported to be one event in 2000 to 3000 anaesthesias. Concerning the aspiration incidence in children compared with adult patients, there are contradictory data in the literature. Several studies suggest that paediatric patients compared to adults have a two- to three-fold higher risk of perioperative pulmonary aspiration.26,36 Other prospective long-term studies did not conrm this increased risk.34,35 Several factors have been identied which are accompanied by an increased risk of aspiration.37e39 These risk factors predisposing to aspiration are summarized in Table 3. Compared to the incidence with elective procedures, the occurrence of a pulmonary aspiration in emergency surgery both in adult patients and in children is clearly increased with 1: 800 and 1: 400, respectively. Additionally, the aspiration risk rises with patients aged over 60. According to Kozlow et al., patients over 80 years have even a nine- to tenfold increased risk of aspiration in comparison to the group of 18- to 29-year-olds.37 It is generally held that obstetric anaesthetic practice is a high-risk area for aspiration and also that the mortality rate is likely to be more frequent during obstetric aspiration than during general surgery.52 Compared to gynaecological patients of similar age, caesarean section patients still have an increased risk of aspiration pneumonitis.53 The decrease in anaesthesia-related maternal death is clearly the result of replacing general anaesthesia by spinal or epidural blocks and standardization of oral sodium citrate as part of preparation for caesarean section. The prevalence of aspiration pneumonia for all surgical patients, stratied by surgical group, is presented in Table 4. The surgical group that had the highest prevalence of aspiration pneumonia involved patients undergoing tracheostomy procedures with 19.1%, compared with an average of 0.7% in patients undergoing procedures other than tracheostomy37, probably because the airway is not protected during the change of cannule. In summary, the total risk of an aspiration seems to be small in elective general surgical patients undergoing general anaesthesia, with a negligible morbidity and mortality.38 Nevertheless, each individual case of aspiration pneumonia, apart from the consequences for the patient, involves also a substantial economic cost factor. The occurrence of aspiration pneumonia is on average associated with a 15-day prolongation of the length of stay in hospital, and additional costs amount to about $22,000, as shown in a study in 52 hospitals in Maryland in the years 1999 and 2000.37 CRICOID PRESSURE Strategies for the prophylaxis of aspiration are repeatedly and comprehensively reviewed in the literature and will not be repeated here.54 The following section focuses more on cricoid pressure as a component of rapid-sequence induction. In general, cricoid pressure is considered a simply accomplished and effective method for the prevention of regurgitation and aspiration of gastric contents.55 This procedure, in which a possible reux is to be prevented by compression of the oesophagus between the

414 M. Janda et al

Table 2. Incidence of aspiration. Reference Country/Period of assessment Study size Patient group Incidence Overall rate 1967e1970, 1975e1983 1975 1975e1983 1985e1991 1967e1976 1978e1982 1984e1988 1989e1993 1978e1982 1985e1997 2000e2002 185.358 338.934 112.721 215.488 240.483 198.103 84.835 85.594 40.240 63.180 24.165 Children/Adults Children/Adults NR Adults NR Children/Adults Children/Adults Children/Adults Children Children Children 1: 2.131 NR 1: 1116 1: 3216 NR 1: 7.335 1:14.139 1: 3.424 1:10.060 1: 2.632 1: 1.272 Emergency procedures Elective procedures 1: 45.454 1: 67.786 NR 1: 71.829 1:240.483 1: 49.525 1: 84.835 No death No death No death No death Mortality

Retrospective study design Olsson26 Sweden Hovi-Viander27 Cohen28 Warner29 Finland Canada USA

Aspiration incidence during emergency procedures was signicantly higher NR NR NR NR 1:895 1:3.886 NR 1-26.5-1.000 NR 1:809 NR 1:373 NR NR 0.4-9.6:1.000 NR 1:3303 NR 1:4.544 NR

Prospective study design South Africa Harrison30 France Tiret31 Leigh32 UK Mellin-Olsen33 Norway Tiret34 France USA Warner35 Murat36 France (NR Not reported).

Management of pulmonary aspiration

415

Table 3. Factors indicating an increased risk for aspiration. Gastric content Delayed gastric emptying (traumatized patients, pyloric spasm, ileus, drugs)26,35 Drugs (opioids, sedatives)39 Increased risk of regurgitation Reux oesophagitis
35,39

Laryngeal incompetence Prehospital intubation46,47

Geriatric patients37,40

General anaesthesia 26,29,31,33,35,39,48 - Emergency surgery 26 - Night-time surgery 29,39,49 - Inadequate anaesthesia Head injury/Trauma26 Neuromuscular disorders/ Neurological decit39,50,51 - Multiple sclerosis - Parkinsons disease - Guillain-Barre - Muscular dystrophies - Cerebral palsy

Gastric hypersecretion (pain, stress)26

Obesity Pro26,39,41 42,43 - Contra Diabetic autonomic neuropathy 44 - Pro 45 - Contra Hiatus hernia39,63
-

ring cartilage and the cervical vertebral bodies, is generally recognized, although a clinical benet of this wide-spread method in the sense of an outcome improvement could not be proven so far in controlled clinical studies. The recommendations regarding the performance of cricoid pressure are thus based on clinical observations as well as on data from studies on animals and cadavers. This is also a reason, however, why there are differing opinions about the efcacy and necessity of cricoid pressure at all as a rm component of rapid-sequence induction. The occurrence of complications is

Table 4. Incidence of aspiration pneumonia by surgical group for 318,880 adult surgical patients in 52 Maryland hospitals, 1999e2000.37 Surgical group Tracheostomies Respiratory system Nervous system Integumentary system Digestive system Nose, mouth, pharynx Hemic and lymphatic system Cardiovascular system Ear Urinary system Musculoskeletal system Male genital system Endocrine system Eye Female genital system Obstetrical procedures Incidence of aspiration pneumonia, % 19.1 2.1 1.4 1.3 1.1 1.1 0.9 0.7 0.7 0.6 0.5 0.3 0.2 0.1 <0.1 <0.1

416 M. Janda et al

rare when indications and contraindications are considered carefully and when the manoeuvre is performed correctly, particularly regarding the force and the duration of application. The work of Vanner et al. provided the pathophysiological background for the requirement of cricoid pressure. They demonstrated that the upper oesophageal sphincter tone decreased in patients after the induction of intravenous anaesthesia with thiopental, midazolam and succinylcholine from on average 39 mmHg in awake condition to less than 10 mmHg, permitting the regurgitation of gastric contents into the pharynx.56 On the other hand, it is well-known that cricoid pressure itself degrades the tone of the lower oesophageal sphincter, probably caused by a pharyngeal reex, and thus alleviates the crossing of gastric contents into the oesophagus.57,58 Goal of this so-called Sellick manoeuvre, which was described by Sellick in 196155, is the compression of the oesophagus between the ring cartilage and the cervical vertebral bodies to prevent a possible reux of gastric contents. With the one-handed variant of this method the thumb and the middle nger are placed on each side of the cricoid cartilage (Figure 1). The index nger should be set above the cartilage to avoid the lateral deviation of the cricoid. Ideally with this procedure a compression of the upper oesophagus sphincters against the sixth cervical vertebral body is reached. The Sellick manoeuvre should begin already with application of the intravenous opiate and hypnotic medication, thus before complete loss of consciousness by the patient, because in this part of anaesthesia induction the sphincter tone already decreases. Vanner et al. showed a reduction of the upper oesophageal sphincter tone

Figure 1. Cricoid pressure (drawing from Sellicks original article, reprinted from The Lancet, Copyright (1961), with permission from Elsevier55).

Management of pulmonary aspiration

417

from an awake value of 43 to 9 mmHg after thiopentone and from 38 to 7 mmHg after midazolam application.56 The force exerted with cricoid pressure is generally indicated in Newton, whereby 9.81 N corresponds to a resting upon weight of 1 kg. Considering that execution of the procedure on the awake patient can cause pain and induce vomiting, the initial force at the time of pre-oxygenation should be restricted to 10 N only. With loss of consciousness by the patient, the force of cricoid pressure should be increased to about 30 N (range 20 N - 40 N).59 This pressure must be maintained continuously until the completion of intubation including blocking of the tube cuff and conrmed endotracheal location of the tube. Crucial for the performance of cricoid pressure is the dosing of the force in order to ensure sufcient aspiration protection, on the one hand, and prevent difculties with laryngoscopy and intubation due to too strong pressure, on the other. The most limiting feature of cricoid pressure is that it can cause anatomical distortion of the upper airway (e.g. pharyngeal compression, distortion/malalignment of the larynx/trachea, activation of upper airway reexes), making airway management more difcult.60 Incorrect application of the manoeuvre may deform the cricoid cartilage, close vocal cords and impair ventilation, especially in female patients.61 Excessive force, wrong (lateral) direction of the force or application of pressure on the larynx rather than on the cricoid ring would make visualization of the larynx and intubation difcult or impossible. On the other hand, cricoid pressure applied correctly by trained personnel does not increase the rate of failed intubation.62 The procedure of cricoid pressure is afrmed with appropriate indication as a preventive method in principle also by paediatric anaesthesiologists63, although the incidence of mechanical airway obstruction is increased due to cricoid pressure straight in infancy.64 Active vomiting leads to a retrograde peristaltic wave, which can lead to an oesophageal rupture when cricoid pressure is maintained. For this reason, cricoid pressure should be released immediately and the head-down position (anti-Trendelenburg position) reverted when active vomiting occurs. Nevertheless, there have been discussions recently as to whether this is justiable in view of the risk of a possible aspiration.65 When the contraindications for the application of cricoid pressure, such as active vomiting, difcult airway conditions, and injuries to the larynx, are considered, serious complications are rare.60 A case report indicates that oesophageal rupture may occur in rapid-sequence induction of anaesthesia for surgery of haematemesis due to a bleeding gastric ulcer.66 This may be due to rapidly increased pressure during vomiting that rupture occurs at the weakest point of the oesophagus, usually on the posterior wall at the extreme lower end.67 Vanner and Pryle59 determined in a study on cadavers that a rupture of the oesophagus occurred in 3 out of 10 cases when cricoid pressure was performed with a force of 30 to 40 N. On the other hand, they showed that with a pressure of 20 N, a strength maximally tolerated by an awake patient, no oesophageal rupture arose. Fracture of the ring cartilage has also been described.68 Several studies in the past have shown that both the knowledge and the technology of cricoid pressure application are rather unsatisfactory under anaesthesiologists and anaesthesia personnel.69e72 Forty per cent of anaesthesiologists in southern Sweden were not aware of possible contraindications to cricoid pressure, and 69% had never heard of force conditions which can be exerted during the cricoid pressure procedure.72 A similar picture emerged under obstetrical anaesthesiologists in France, half of whom were not able to describe the technology of applying cricoid pressure correctly.69 According to available data, it is doubtful whether cricoid pressure is always correctly accomplished in practice, regarding its execution, the force employment and

418 M. Janda et al

the temporal operational sequence during the rapid-sequence induction. Under the criterion of rising complications due to inaccurate performance, i.e., with an increase of risk instead of usefulness as a consequence of ineffective application, it is necessary to train medical and nursing personnel on a regular and purposeful basis as a precondition for correct application of cricoid pressure. On the other hand, this could be a starting point for a critical discussion about a clinically established method which so far has not been shown to exert a positive effect on the outcome of the patient. TREATMENT OF ASPIRATION Principles of crisis management The management of critical events is one of the most challenging and important tasks an anaesthesiologist can face in clinical practice. For successful incident management in anaesthesia, dynamic decision-making with the application of prepared algorithms is necessary. According to Gaba et al.73, the basic principles of medical crisis management are based on the following components: Observation Clinical observation of the patient using the monitoring available as well as verication of the observations made. Decisions Problem recognition and forecast of the further process (situation assessment). Act Application of prepared algorithms. Re-evaluation Actualization of the estimate of the situation, questioning of the effectiveness of the assigned procedures. Recalling such a structural procedure should be the basis of managing an acute pulmonary aspiration arising during general anaesthesia. Kluger et al. showed that the correct application of an explicit algorithm during the occurrence of aspiration led to earlier recognition and/or to better management of the problem in 19% of cases.74 Practical procedure The rst step for the successful management of an aspiration is immediate recognition of the occurrence of gastric contents in the oropharynx or the airways (observation). Symptoms which indicate an aspiration of gastric contents are:
-

Visible gastric contents in the oropharynx Appearance of hypoxia despite correct endotracheal intubation and ventilation Increased inspiratory pressure during mechanical ventilation

Management of pulmonary aspiration

-

419

Dyspnea, apnea or hyperventilation during spontaneous breathing Bronchospasm, laryngospasm Auscultatory abnormalities Inspection: thorax collections

Particularly after covert pulmonary aspiration of gastric contents, these symptoms must be dened rst against similar differential-diagnostical events (decisions). Bronchospasm, pulmonary edema, ARDS, pulmonary embolism, and obstruction of the endotracheal tube can produce a similar respiratory picture as aspiration. In a study from Australia, the diagnosis of regurgitation, vomiting, and aspiration was conrmed by clinical observation in 70% of 183 relevant incidents among 4000 reports, whereas in 15% of the cases aspiration occurred primarily as an unexplained decrease in saturation, in 6% as laryngospasm, in 3% as obstruction of the airway, in 2% as bronchospasm and in 1% with hyperventilation, while 1% were accompanied by a difcult intubation, and 0.5% of the cases occurred with pulmonary edema as well as cardiac arrest.74 If the diagnosis of aspiration is suspected, the following procedures should be done and adapted to the situation (to act). If a pulmonary aspiration was already recognized during induction of anaesthesia and/or during laryngoscopy, immediate endotracheal suctioning is indicated, followed by an immediate orotracheal intubation in form of a rapid-sequence induction. Each of the following manoeuvres should be performed considering the following principle: no unnecessary time may be lost with respect to a possibly dropping oxygen saturation of the patient. Highest priority in this situation is the maintenance of an adequate oxygenation of the patient. For this, a controlled ventilation with an inspiratory oxygen fraction of 1.0 should be accomplished and a positive endexpiratory airway pressure (PEEP) should be installed at least at about 5 cmH2O.75 In case aspiration occurs after completing the intubation, the patient should be brought immediately into a head-down position. An endotracheal suctioning by the tube using a large suction catheter is indicated. A lavage over the tube is usually not indicated after the aspiration of liquids, for example of pure gastric acid, since by this procedure a distribution of the aspirate into deeper, peripheral lung sections can be provoked. If the aspiration of particulated matter is assumed, a bronchoscopy should be performed. The careful elimination of all particles with exible bre optics is recommended, while samples of the lung aspirates should be taken for determination of the pH as well as for a microbiological diagnosis. Larger rm particles must in any case be removed by bronchoscopy in order to prevent the development of airway obstruction with atelectases distal to the foreign body. The further treatment of pulmonary aspiration is adjusted to subsequent symptoms. The occurrence of a bronchospasm has to be treated symptomatically. For this, the application of a systemic (theophylline) or topical (salbutamol) bronchodilator can be helpful for the dilatation of larger, spastic airways in less damaged lung areas which are constricted due to a reex mechanism. However, the use of the bronchodilatory effect of inhalation anaesthetics should be avoided after an acid-associated aspiration in the context of a general anaesthesia, since there are data suggesting a reinforcement of acute inammatory reaction e.g. by isourane, enurane, and halothane.76 A sufcient uid management is essential as accompanying therapy, since volume shifts with consecutive haemodynamic changes may occur following a developing pulmonary edema.

420 M. Janda et al

After successful management of the initial phase following pulmonary aspiration, the progress of the planned operation has to be discussed in consent with the surgical colleagues. Here elective surgery should be cancelled wherever possible and emergency surgery should be limited to the smallest procedure which is compatible with the patients security. Each action should be accompanied by tight control of the situation and the question should be asked as to whether the condition of the patient has improved or whether further actions are required (re-evaluation). According to the severity of aspiration, frequent arterial blood gas analyses should be performed in order to optimize mechanical ventilation by adjusting the inspiratory oxygen concentration, the respiratory rate, and the PEEP level. A chest X-ray should be done as soon as possible in any case of suspected pulmonary aspiration to specify the pulmonary pathology. However, it must be pointed out that in approximately 25% of cases radiographic signs of an aspiration are missing initially. Patients with an asymptomatic course two hours after the event can be transferred to a normal ward after a follow-up visit has been arranged. Warner et al. showed in a retrospective study that such patients neither showed respiratory consequences later nor required further postoperative interventions.29 Patients who are stable after extubation during a period of two hours in the recovery room (oxygen saturation at least 95% under an FiO2 < 0.5, heart rate <100/min, respiration rate <20/min in adults), who have no bronchospasm or fever and who are without pathological changes in their chest X-ray compared to the preoperative ndings can likewise be transferred to the normal ward.74 All other patients who do not full the aforementioned criteria should be transferred to an intensive care unit for further observation and therapy. In the study of Warner, 18 out of 66 patients (27.3%) who had aspirated had to be further treated with ventilatory support on an ICU.29 Antibiotic therapy The use of mandatory treatment with antibiotics after the aspiration of gastric contents is debated in the literature. Although published guidelines exist for nosocomialacquired pneumonia77, there are no denitive guidelines available for antibiotic treatment of suspected or conrmed aspiration, primarily concerning timing and choice of antimicrobial agents. According to current knowledge, antibiotics should not be given in the acute phase of aspiration for the following reasons: a routine antibiotic therapy has no obviously positive inuence on the clinical outcome of the patients or on the further disease process.78 The primary injury to the lung mainly concerns a chemical impairment; bacteria do not play a role in this acute phase.79 However, approximately 20% to 30% of patients develop a subsequent infection80, since the lung is more susceptible to bacteria after damage due to aspiration.81 However, prophylactic antibiotic application, i.e. before the beginning of pneumonia, has been shown to lead to an increased incidence of ventilator-associated pneumonias due to virulent pathogens, such as pseudomonas aeruginosa and acinetobacter species.54 In conclusion, the application of antibiotics should be delayed until the pathogenic germs are specied82,83 and/or until signs of secondary bacterial infections are present. The inappropriate practice of administering empirical antibiotics for aspiration without a clear microbial component must be strongly discouraged in view of evidence-based medicine.24

Management of pulmonary aspiration

421

Nevertheless, antibiotics are nowadays often applied before the isolation of germs, although larger controlled studies of empirical or calculated antibiotic therapy in the context of pulmonary aspiration have not been done. A national survey in the United States of America performed in 2001 conrmed this procedure. 51.9% of physicians started administering antibiotics already at the suspicion of an aspiration, and 77.7% with conrmed aspiration before denite proof of an infection. In the context of the treatment of denite aspiration pneumonia, 27.6% of physicians preferred a pathogen specic therapy, whereas 72.4% chose the antibiotic empirically.24 If the initiation of an antibiotic therapy seems to be necessary due to the clinical progress before the proof of a germ, the choice of the antibiotic therapy should be based on the clinical condition of the patient and on the typical spectrum suspected in aspiration pneumonia acquired in the particular hospital. Penicillin and clindamycin are frequently used as rst-line antibiotics for the empirical treatment of aspiration pneumonia under the assumption of a mixed aerobic/anaerobic germ spectrum.24 Penicillin is often combined with a b-lactamase-inhibitor (for example amoxicillin/ clavulanic acid). Alternatively, a combination of a third-generation cephalosporin (for example ceftriaxon) with clindamycin is recommended. Both combinations seem equally effective.84,85 Due to the fact that anaerobes possibly no longer take the predominant place in the spectrum of the pathogenic germs, a change in the antibiotic strategy seems to be indicated.23 Antibiotics with effectiveness against gram-negative bacteria, like third-generation cephalosporins or uoroquinolones, gain importance in this context.17 However, structured clinical pathways that account for the cost-effectiveness of delaying initial antimicrobial therapy until an aspiration diagnosis is documented, along with the actual impact on mortality rate, are desperately needed.24 Corticoid therapy There is no evidence that the routine intravenous application of steroids has a place in the management of pulmonary aspiration. A reduction and/or inhibition of the inammatory reaction in the acute phase by application of high-dose corticoid steroids has not been conrmed in these patients.86e92 On the contrary, the use of steroids can even have an unfavourable effect on the mortality of critically ill patients.86,87 Hence, corticosteroids should not be given prophylactically in the acute phase of aspiration.81 Altogether the management of pulmonary aspiration is nonspecic and adjuvant. Future research work should focus on the development of intratracheally12 or intravenously applicable drugs for the neutralization of the effects caused by the aspiration of particulate matter, particularly with low pH values. Until today, an effective pharmacological therapy for patients after acid aspiration has not been established despite its enormous clinical relevance due to the mortality of aspiration pneumonitis.17 Animal studies have shown some promising results. The early application of the phosphodiesterase inhibitor pentoxifylline improved oxygenation by reducing the release of the proinammatory cytokine TNF -a in rats. Additionally, pentoxifylline signicantly increased survival rate probably due to its additional inotropic effect.93 Also the application of thymoquinon, an extract from black cumin (Nigella sativa) with anti-inammatory, bronchodilatory and antibacterial effects, provided better oxygenation as well as histopathologically smaller damage to the lung tissue in the rat.94

422 M. Janda et al

SUMMARY The aspiration of gastric contents can cause a broad spectrum of symptoms and clinical outcomes, ranging from mild asymptomatic and in themselves limited episodes up to the development of a severe pneumonitis with transition to an acute respiratory distress syndrome (ARDS). For the management of pulmonary aspiration, differentiation between aspiration pneumonitis and aspiration pneumonia is of crucial importance. The incidence of aspiration during elective surgery amounts to 1 per 2000e3000 anaesthesias for adults and 1 per 1200e2600 anaesthesias in children. In emergency surgery the incidence is three to four times higher. The risk is particularly increased in non-fasting patients, older patients, and pregnant women, in abdominal surgery, and in consciousness-reduced patients. The prevention of an aspiration is of crucial importance. For this purpose, rapidsequence-induction techniques are used, which are clinically common and widely accepted, although their use has not been conrmed in the sense of an outcome improvement for the patients. Future studies should aim at the evaluation of manoeuvres like the optimal position of the patient during rapid-sequence induction or the efcacy of cricoid pressure. The therapy of conrmed aspiration is symptomatic and adjunctive, whereby the main goal is the maintenance of an adequate oxygenation. The application of corticosteroids and/or antibiotics should be omitted in the acute phase, since there is no evidence of an outcome improvement. Pulmonary aspiration should be treated using explicit algorithms which have been shown to accelerate problem recognition and improve therapy. However, further research is necessary to support this strategy.

Practice points Algorithm following the Crisis management manual of the Australian Patient Safety Foundation95 1. Management of regurgitation and vomiting  Head down, lateral posture, if feasible  Try to clear and suction the airway  Give 100% oxygen  Consider deepening anaesthesia to visualize and clear the pharynx/airway  Ventilate the lungs while cricoid pressure is maintained  Give suxamethonium and intubate the trachea under cricoid pressure 2. Diagnosis of Aspiration e Aspiration signs  Laryngospasm/airway obstruction  Bronchospasm/wheezing/crackles  Hypoventilation/dyspnea/apnea  Reduced compliance (ARDS)  Desaturation/bradycardia/cardiac arrest

Management of pulmonary aspiration

423

3. Further Care e Operation room  Information to the surgeon  Sedation, analgesia  Mechanical ventilation via endotracheal tube (FiO2 1.0; PEEP 5e7 cmH2O)  Suction airway, bronchoscopy if necessary  Systemic (theophylline) or topical (salbutamol) bronchodilators as necessary  Fluid therapy to maintain normovolaemic state  Steroids and antibiotics should not be used early or routinely.  Chest X-ray. If normal, and if saturation is adequate, extubate.  If stable after 2 hr in recovery room, send to the ward and arrange for follow up visits.  If unstable or saturation is inadequate maintain intubation and PEEP and admit to a high dependency area. 4. Further Care e ICU  Repeat chest X-ray and blood gases  Consider PEEP, bronchodilators, inotropes, uids  Culture sputum and tracheal aspirates  Give antibiotics on the basis of culture results (germ specic)  Reassess daily

Research agenda  Development of a risk score for the determination of the probability of aspiration on the basis of well-known risk factors  Proof of efciency of different measures/strategies in the course of the rapid sequence induction as for example of the application of the cricoid pressure or different storage techniques (head high and/or head down position)  Evaluation of the current routine procedure offer the occurrence of an aspiration in the form of surveys or prospective multi-center studies  Development of algorithms for the management of aspiration based on evidencebased data and evaluation of these algorithms with special respect to outcome

REFERENCES
1. Rotta AT, Shiley KT, Davidson BA et al. Gastric acid and particulate aspiration injury inhibits pulmonary bacteria clearance. Critical Care Medicine 2004; 32: 747e754. 2. Ljungqvist O & Soreide E. Preoperative fasting. The British Journal of Surgery 2003; 90: 400e406. 3. Mendelson C. The aspiration of stomach contents into the lungs during obstetric anesthesia. American Journal of Obstetrics and Gynecology 1946; 52: 191e205. 4. Exarhos ND, Logan WJ, Abott OA & Hatcher Jr. CR. The importance of pH and volume in tracheobronchial aspiration. Diseases of the Chest 1965; 47: 167e169. 5. Roberts RB & Shirley MA. Reducing the risk of acid aspiration during cesarean section. Anesthesia and Analgesia 1974; 53: 859e868. 6. Knight PR, Davidson BA, Nader ND et al. Progressive, severe lung injury secondary to the interaction of insults in gastric aspiration. Experimental Lung Research 2004; 30: 535e557.

424 M. Janda et al 7. Knight PR, Rutter T, Tait AR et al. Pathogenesis of gastric particulate lung injury: a comparison and interaction with acidic pneumonitis. Anesthesia and Analgesia 1993; 77: 754e760. 8. James CF, Modell JH, Gibbs CP et al. Pulmonary aspiration e effects of volume and pH in the rat. Anesthesia and Analgesia 1984; 63: 665e668. 9. Porembka DT, Kier A, Sehlhorst S et al. The pathophysiologic changes following bile aspiration in a porcine lung model. Chest 1993; 104: 919e924. 10. Warner MA, Caplan RA, Epstein BS et al. Practice guidelines for preoperative fasting and the use of pharmacological agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures: a report by the American Society of Anesthesiologists Task Force on Preoperative Fasting. Anesthesiology 1999; 90: 896e905. *11. Kennedy TP, Johnson KJ, Kunkel RG et al. Acute acid aspiration lung injury in the rat: biphasic pathogenesis. Anesthesia and Analgesia 1989; 69: 87e92. 12. Beck-Schimmer B, Rosenberger DS, Neff SB et al. Pulmonary aspiration. New therapeutic approaches in the experimental model. Anesthesiology 2005; 103: 556e566. 13. Davidson BA, Knight PR, Helinski JD et al. The role of tumor necrosis factor-alpha in the pathogenesis of aspiration pneumonitis in rats. Anesthesiology 1999; 91: 486e499. 14. Nemzek JA, Call DR, Ebong SJ et al. Immunopathology of a two-hit murine model of acid aspiration lung injury. American Journal of Physiology 2000; 2778: L512eL520. 15. Knight PR, Druskovich G, Tait AR & Johnson KJ. The role of neutrophils oxidants, and proteases in the pathogenesis of acid pulmonary injury. Anesthesiology 1992; 77: 772e778. 16. Nemzek JA. Mechanistic approaches to acid aspiration and pneumonia must look beyond tumor necrosis factor-a levels. Critical Care Medicine 2005; 33: 1877e1878. *17. Marik PE. Aspiration pneumonitis and aspiration pneumonia. The New England Journal of Medicine 2001; 344: 665e671. 18. Westerloo DJ, Knapp S, vant Veer C et al. Aspiration pneumonitis primes the host for an exaggerated inammatory response during pneumonia. Critical Care Medicine 2005; 33: 1770e1778. 19. Lorber B & Swenson RM. Bacteriology of aspiration pneumonia. A prospective study of communityand hospital-acquired cases. Annals of Internal Medicine 1974; 81: 329e331. 20. Bartlett JG, Gorbach SL & Finegold SM. The bacteriology of aspiration pneumonia. The American Journal of Medicine 1974; 56: 202e207. 21. Bartlett JG & Gorbach SL. The triple threat of aspiration pneumonia. Chest 1975; 68: 560e566. 22. Mackowiak PA. The normal microbial ora. The New England Journal of Medicine 1982; 307: 83e86. 23. Marik PE & Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia. Chest 1999; 115: 178e183. 24. Rebuck JA, Rasmussen JR & Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Critical Care Medicine 2001; 21: 2239e2244. 25. Webb RK, van der Walt JH, Runciman WB et al. The Australian incident monitoring study. Which monitor? An analysis of 2000 incident reports. Anaesthesia and Intensive Care 1993; 21: 529e542. *26. Olsson GL, Hallen B & Hambraeus-Jonzon K. Aspiration during anaesthesia: a computer-aided study of 185358 anaesthetics. Acta Anaesthesiologica Scandinavica 1986; 30: 84e92. 27. Hovi-Viander M. Death associated with anaesthesia in Finland. British Journal of Anaesthesia 1980; 52: 483e489. 28. Cohen MM, Duncan PG, Pope WD & Wolkenstein C. A survey of 112.000 anaesthetics at one teaching hospital (1975e1983). Canadian Anaesthetists Society Journal 1986; 33: 22e31. *29. Warner MA, Warner ME & Weber JG. Clinical signicance of pulmonary aspiration during the perioperative period. Anesthesiology 1993; 78: 56e62. 30. Harrison GG. Death attributable to anaesthesia. A 10-year survey (1967e1976). British Journal of Anaesthesia 1978; 50: 1041e1046. 31. Tiret L & Hatton F. Complications associated with anaesthesia e a prospective survey in France. Canadian Anaesthetists Society Journal 1986; 33: 336e344. 32. Leigh JM & Tytler JA. Admissions to the intensive care unit after complications of anaesthetic techniques over 10 years. 2. The second 5 years. Anaesthesia 1990; 45: 814e820. 33. 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 Anaesthesiologica Scandinavica 1996; 40: 1184e1188.

Management of pulmonary aspiration

425

34. Tiret L, Nivoche Y, Hatton F & Desmonts JM. Complications related to anaesthesia in infants and children. A prospective survey of 40.240 anaesthatics. British Journal of Anaesthesia 1988; 61: 263e269. 35. Warner MA, Warner ME, Warner DO et al. Perioperative pulmonary aspiration in infants and children. Anesthesiology 1999; 90: 66e71. 36. Murat I, Constant I & MaudHuy H. Perioperative anaesthetic morbidity in children: a database of 24165 anaesthetics over a 30-month period. Paediatric Anaesthesia 2004; 14: 158e166. 37. Kozlow JH, Berenholtz SM, Garrett E et al. Epidemiology and impact of aspiration pneumonia in patients undergoing in Maryland. Critical Care Medicine 2003; 31: 1930e1937. *38. Engelhardt T & Webster NR. Pulmonary aspiration of gastric contents in anaesthesia. British Journal of Anaesthesia 1999; 83: 453e460. 39. Kluger MT & Short TG. Aspiration during anaesthesia: a review of 133 cases from the Australian Anaesthetic Incident Monitoring Study (AIMS). Anaesthesia 1999; 54: 19e26. 40. Kikawada M, Iwamoto T & Takasaki M. Aspiration and infection in the elderly: epidemiology, diagnosis and management. Drugs & Aging 2005; 22: 115e130. 41. Vaughan RW, Bauer S & Wise L. Volume and pH of gastric juice in obese patients. Anesthesiology 1975; 43: 686e689. 42. Harter RL, Kelly WB, Kramer MG et al. A comparison of the volume and pH of gastric contents of obese and lean surgical patients. Anesthesia and Analgesia 1998; 86: 147e152. 43. Zacchi P, Mearin F, Humbert P et al. Effect of obesity on gastroesophageal resistance to ow in man. Digestive Diseases and Sciences 1991; 36: 1473e1480. 44. Ishihara H, Singh H & Giesecke AH. Relationship between diabetic autonomic neuropathy and gastric contents. Anesthesia and Analgesia 1994; 78: 943e947. 45. Jellish WS, Kartha V, Fluder E & Slogoff S. Effect of metoclopramide on gastric uid volumes in diabetic patients who have fasted before elective surgery. Anesthesiology 2005; 102: 904e909. 46. Lockey DJ, Coats T & Parr MJ. Aspiration in severe trauma: a prospective study. Anaesthesia 1999; 54: 1097e1098. 47. Ufberg JW, Bushra JS, Karras DJ et al. Aspiration of gastric contents: association with prehospital intubation. The American Journal of Emergency Medicine 2005; 23: 379e382. 48. Borland LM, Sereika SM, Woelfel SK et al. Pulmonary aspiration in pediatric patients during general anesthesia: incidence and outcome. Journal of Clinical Anesthesia 1998; 10: 95e102. 49. Brimacombe JR & Berry A. The incidence of aspiration associated with the laryngeal mask airway: a meta-analysis of published literature. Journal of Clinical Anesthesia 1995; 7: 297e305. 50. Bulat RS & Orlando RC. Oropharyngeal dysphagia. Current Treatment Options in Gastroenterology 2005; 8: 269e274. 51. Spiroglou K, Xinias I, Karatzas N et al. Gastric emptying in children with cerebral palsy and gastroesophageal reux. Pediatric Neurology 2004; 31: 177e182. 52. Ng A & Schmith G. Gastroesophageal reux and aspiration of gastric contents in anesthetic practice. Anesthesia and Analgesia 2001; 93: 494e513. 53. Soreide E, Bjornestad E & Steen PA. An audit of perioperative aspiration pneumonitis in gynaecological and obstetric patients. Acta Anaesthesiologica Scandinavica 1996; 40: 14e19. *54. Kalinowski CPH & Kirsch JR. Strategies fu r prophylaxis and treatment for aspiration. Best Practice & Research. Clinical Anaesthesiology 2004; 18: 719e737. 55. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961; 2: 404e406. 56. Vanner RG, Pryle BJ, ODwyer JP & Reynold F. Upper oesophageal sphincter pressure and the intravenous induction of anaesthesia. Anaesthesia 1992; 47: 371e375. treau P. Cricoid pressure decrease lower oesophageal 57. Chassard D, Tournadre JP, Berrada K & Boule sphincter tone in anaesthetized pigs. Canadian Journal of Anaesthesia 1996; 43: 414e417. treau P. Lower oesophageal sphincter pressure during 58. Tournadre JP, Chassard D, Berrada K & Boule application of cricoid pressure in conscious volunteers. British Journal of Anaesthesia 1996; 76: A50. 59. Vanner RG & Pryle BJ. Regurgitation and oesophageal rupture with cricoid pressure: a cadaver study. Anaesthesia 1992; 47: 732e735. 60. Brimacombe JR & Berry AM. Cricoid pressure. Canadian Journal of Anaesthesia 1997; 44: 414e425. 61. MacG Palmer JH & Ball DR. The effect of cricoid pressure on the cricoid cartilage and vocal cords: an endoscopic study in anaesthetized patients. Anaesthesia 2000; 55: 263e268.

426 M. Janda et al panier CA et al. Cricoid pressure does not increase the rate of failed 62. Turgeon AF, Nicole PC, Tre intubation by direct laryngoscopy in adults. Anesthesiology 2005; 102: 315e319. 63. Engelhardt T, Strachan L & Johnston G. Aspiration and regurgitation prophylaxis in paediatric anaesthesia. Paediatric Anaesthesia 2001; 11: 147e150. 64. Moynihan RJ, Brock-Utne JG, Archer JH et al. The effect of cricoid pressure on preventing gastric insufation in infants and children. Anesthesiology 1993; 78: 652e656. 65. Notcutt W. Oesophageal rupture and cricoid pressure. Anaesthesia 1991; 46: 424e425. 66. Ralph SJ & Wareham CA. Rupture of the oesophagus during cricoid pressure. Anaesthesia 1991; 46: 40e41. 67. The oesophagus. In Harding-Rains AJ & Mann CV (eds.). Bailey and Loves Short Practice of Surgery. 20th edn. London: H.K. Lewis & Co Ltd, 1988, pp. 827e854. 68. Heath KJ, Palmer M & Fletcher SJ. Fracture of the cricoid cartilage after Sellicks manoeuvre. British Journal of Anaesthesia 1996; 76: 877e878. 69. Benhamou D. French obstetric anaesthesists and acid aspiration prophylaxis. European Journal of Anaesthesiology 1993; 10: 27e32. 70. Meek T, Gittins N & Duggan JE. Cricoid pressure: knowledge and performance amongst anaesthetic assistants. Anaesthesia 1999; 54: 59e62. 71. Morris J & Cook TM. Rapid sequence induction: a national survey of practice. Anaesthesia 2001; 56: 1090e1097. 72. Schmidt A & Akeson J. Practice and knowledge of cricoid pressure in southern Sweden. Acta Anaesthesiologica Scandinavica 2001; 45: 1210e1214. *73. Gaba DM, Fish KJ & Howard SK. Crisis Management in Anesthesiology. New York e Edinburgh e LondonMelbourne e Madrid e Tokyo: Churchill Livingstone Inc; 1994, pp. 18e25. 74. Kluger MT, Visvanathan T, Myburgh JA & Westhorpe RN. Crisis management during anaesthesia: regurgitation, vomiting, and aspiration. Quality & Safety in Health Care 2005; 14: e4. 75. Peitzman AB, Shires 3rd GT, Illner H & Shires GT. Pulmonary acid injury: effects of positive endexpiratory pressure and crystalloid vs colloid uid resuscitation. Archives of Surgery 1982; 117: 662e668. 76. Nader-Djalal N, Knight PR, Bacon MF et al. Alterations in the course of acid-induced lung injury in rats after general anesthesia: volatile anesthetics versus ketamine. Anesthesia and Analgesia 1998; 86: 141e146. 77. American Thoracic Society & Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. American Journal of Respiratory and Critical Care Medicine 2005; 171: 388e416. 78. Bynum LJ & Pierce AK. Pulmonary aspiration of gastric content. The American Review of Respiratory Disease 1976; 114: 1129e1136. 79. LeFrock JL, Clark TS, Davies B & Klainer AS. Aspiration pneumonia: a ten-year review. The American Surgeon 1979; 45: 305e313. 80. Hall JB, Schmidt GA & Wood LDH (eds.). Principles of Critical Care. Aspiration Syndromes. New York: McGraw-Hill; 1992. 81. DePaso WJ. Aspiration pneumonia. Clinics in Chest Medicine 1991; 12: 269e284. 82. Hickling KG & Howard R. A retrospective survey of treatment and mortality in aspiration pneumonia. Intensive Care Medicine 1988; 14: 617e622. 83. Janknegt R, Wijnands WJA & Stobberingh EE. Antimicrobial practice. Antibiotic policies in Dutch hospitals for treatment of pneumonia. The Journal of Antimicrobial Chemotherapy 1994; 34: 431e442. 84. Allewelt M, Schuler P, Boleskei PL et al. Ampicillin sulbactam vs. clindamycin / cephalosporin for the treatment of aspiration pneumonia and primary lung abscess. Clinical Microbiology and Infection 2004; 10: 163e170. 85. Jacobson SJ, Grifths K, Diamond S et al. A randomized controlled trial of penicillin vs clindamycin for the treatment of aspiration pneumonia in children. Archives of Pediatrics & Adolescent Medicine 1997; 151: 701e704. 86. Wynne JW, Reynolds JC, Hood I et al. Steroid therapy for pneumonitis induced in rabbits by aspiration of foodstuff. Anesthesiology 1979; 51: 11e19. 87. Sukumaran M, Granada MJ, Berger HW et al. Evaluation of corticosteroid treatment in aspiration of gastric contents: a controlled clinical trial. The Mount Sinai Journal of Medicine, New York 1980; 47: 335e340.

Management of pulmonary aspiration

427

88. Wolfe JE, Bone RC & Ruth WE. Effects of corticoids in the treatment of patients with gastric aspiration. The American Journal of Medicine 1977; 63: 719e722. 89. Gates S, Huang T & Cheney FW. Effects of methylprednisolone on resolution of acid-aspiration pneumonitis. Archives of Surgery 1983; 118: 1262e1265. 90. Peitzman AB, Shires 3rd GT, Illner H & Shires GT. The effect of intravenous steroids on alveolarcapillary membrane permeability in pulmonary acid injury. The Journal of Trauma 1982; 22: 347e352. 91. Bone RC, Fisher CJ, Clemmer TP et al. A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. The New England Journal of Medicine 1987; 317: 653e658. 92. Lefering R & Neugebauer AEM. Steroid controversy in sepsis and septic shock: a meta analysis. Critical Care Medicine 1995; 23: 1294e1303. 93. Pawlik MT, Schreyer AG, Ittner KP et al. Early treatment with pentoxifylline reduces lung injury induced by acid aspiration in rats. Chest 2005; 127: 613e621. 94. Isik AF, Kati I, Bayram I & Ozbek H. A new agent for treatment of acute respiratory distress syndrom: thymoquinone. An experimental study in a rat model. European Journal of Cardio-thoracic Surgery 2005; 28: 301e305. *95. Australian Patient Safety Foundation. Crisis Management Manual: COVER ABCD A SWIFT CHECK. Adelaide: Australian Patient Safety Foundation; 1996. 74 pp. Available at http://www.apsf.net.au/ anaesthesia.htm.