4 manejo aspiracion pulmonar

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4

Management of pulmonary aspiration

Matthias Janda* MDConsultant Anaesthetist

Thomas W.L. Scheeren MDProfessor of Anaesthesiology

Gabriele F.E. Noldge-Schomburg MDProfessor of Anaesthesiology and Chair

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 increasedpostoperative morbidity and mortality. For the management of aspiration, differentiationbetween acid-associated aspiration pneumonitis and aspiration pneumonia as a consequenceof a secondary bacterial contamination is of crucial importance.

The incidence of aspiration in elective surgery is 1 per 2000e3000 anaesthesias in adults. Inchildren, it is slightly more common with 1 per 1200e2600 anaesthesias. In the context of emer-gency anaesthesias the incidence of aspiration is three to four times higher. The risk particularlyincreases with recent ingestion of solid food or fluids, with older patients, with pregnant women,and with consciousness-reduced patients. Besides giving a review of the pathophysiology, inci-dence, and the risk factors of aspiration, this article places emphasis on the practical manage-ment of this anaesthesia-associated complication. Cricoid pressure, as a non-evidence-basedbut 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 byuse of scientific concepts based on medical crisis management. For this, an algorithm basedon current scientific investigations is presented.

Key words: pulmonary aspiration; aspiration pneumonitis; aspiration pneumonia; cricoidpressure; rapid sequence induction; crisis management; treatment of aspiration.

* Corresponding author. Tel.: 49 381 494 6401; Fax: 49 381 494 6402.

E-mail address: [email protected] (M. Janda).

1521-6896/$ - see front matter 2006 Elsevier Ltd. All rights reserved.

Best Practice & Research Clinical AnaesthesiologyVol. 20, No. 3, pp. 409e427, 2006

doi:10.1016/j.bpa.2006.02.006

available online at http://www.sciencedirect.com
mailto:[email protected]://www.sciencedirect.com/http://www.sciencedirect.com/mailto:[email protected]


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The aspiration of gastric contents is associated with a broad spectrum of possible clin-ical outcomes, ranging from mild asymptomatic and in themselves limited episodes ofbronchial irritation up to the development of a severe pneumonitis with transition toan acute respiratory distress syndrome (ARDS).1

The pathogenesis of aspiration pneumonitis and aspiration pneumonia has been suf-ficiently clarified in the last few years, particularly in fundamental animal experiments.

Surveys on the incidence and predisposing risk factors focused on particularly endan-gered patient collectives (emergency room admissions with higher ASA classification,pregnant women, patients with recent ingestion of solid food or fluids, geriatric pa-tients, and consciousness-reduced patients) and promoted the development of appro-priate strategies for the prophylaxis of aspiration causing secondary morbidity andcomplications.

Several randomized controlled studies in healthy adults undergoing elective surgeryhave reported that oral intake of clear fluids up to 2 hr before anaesthesia inductionoccurs does not increase gastric fluid 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, how-ever, is still limited primarily to a supporting therapy.

Controlled studies of the gradual management of pulmonary aspiration do not yetexist. The use of evidence-based algorithms in the context of recognizing and treatingaspiration could arrange the therapy more efficiently and improve the patientsoutcome.

PATHOPHYSIOLOGY

Aspiration is defined as the entry of liquid or particulate matter into the tracheobron-chial tree, as a consequence of passive regurgitation or active vomiting of gastric con-tents from patients without sufficient laryngeal protection reflexes. Depending uponcondition and composition of the aspirates, three different complications can be differ-entiated as a consequence of a pulmonary aspiration, without a strict demarcation inclinical practice:

1. acid-associated aspiration pneumonitis,2. bacterial infection,3. particle-associated aspiration.

1. Aspiration pneumonitis as a result of an acid-associated aspirationThe classical aspiration pneumonia, the so-called Mendelson syndrome, was de-scribed by Mendelson in 1946 for the first time.3 Here it concerns a chemical dam-age 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/orcontents occurring depends strongly on the pH value and on the quantity of the as-pirate.4 However, the concept of critical borders described previously (pH value ofthe 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 theinterrelationship of the factors pH value, volume, and presence of particles is ofimportance.6,7 Already small volumes can cause a high mortality rate if the pH valueis very low. On the other hand, a higher volume can be tolerated if the gastric liquid

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is effectively buffered.8 Furthermore, in the pig model it was shown that the aspira-tion of bile acid with a pH of 7.19 leads to more serious physiological and histolog-ical 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 acidaspiration 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 proceedsin two phases.11 The first phase is marked by a physiochemical process, which leadsto direct toxic damage to the respiratory epithelium by the acid. Injury to thealveolo-capillary barrier with deletion of the type I-cells of the alveolar epitheliumresults in severe damage to the lung endothelium. An increased alveolar permeabil-ity leads to diffuse alveolar infiltration with the development of an interstitialpulmonary edema. As a consequence, the lung compliance decreases and a mis-match 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 inflammatory reaction. Inflamma-tory cytokines play a central role as mediators for the lung parenchyma damage dueto aspiration of acidic gastric contents. Interleukin-1b and tumor necrosis factora are released by stimulated alveolar macrophages12 and stand as early responsecytokines at the beginning of the inflammatory cascade.6,13 They induce theproduction of further cytokines (e.g. IL-10) and chemokines (e.g. monocyte chemo-attractant protein 1 [MCP-1], macrophage inflammatory protein 1b [MIP-1b]),cytokine-induced neutrophil chemoattractant 1 [CINC-1], and macrophage inflam-matory protein 2 [MIP-2] by macrophages and mesenchymale cells.1,6,14 Neutro-phils play a key role in the development of the lung injury also by the release of

oxygen radicals and proteases.15,16Clinically, aspiration pneumonitis can proceed both asymptomatically and in therange of a non-productive cough up to tachypnoea, bronchospasm, bloody cough,and the development of a respiratory insufficiency 2 to 5 hr after the aspiration.17

2. Aspiration pneumonia as a consequence of a secondary bacterial infectionAspiration pneumonia is an infectious process, which is a consequence of the inha-lation of oropharyngeal secretion or gastric contents contaminated with pathogenicbacteria. An acid-associated aspiration pneumonitis, on the other hand, favours thesecondary development of aspiration pneumonia by superinfection with bacteria

due to the destroyed respiratory epithelium.1,18

Although there is some overlapbetween aspiration pneumonitis and aspiration pneumonia, they are distinct clinicalentities shown by Marik in Table 1.17

The composite of the aspirate depends on the germ spectrum in the particularhospital. Earlier studies of the germ spectrum of aspiration pneumonia identified an-aerobic species as the typical pathogenic germs19e21, since these were isolated fre-quently from the oropharyngeal flora.22 Recent studies, however, have called intoquestion the pathogenic role of aerobes in the context of aspiration pneumonia.23,24

Staphylococcus aureus (both methicilline sensitive and methicilline resistant), pseu-domonas aeruginosa, enterobacter species, anaerobes, klebsiella species and escher-

ichia coli rank among the most frequent pathogenic bacteria, without a dominance ofan individual germ given.23,24

The aspiration event is often not observed. Especially in intensive care with long-term ventilatory support, silent aspiration occurs more frequently despite the use

Management of pulmonary aspiration 411


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of cuffed tubes. Clinically, aspiration pneumonia is evidenced by coughs andtachypnea 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 radio-graphic evidence of an infiltrate in a characteristic bronchopulmonary segment.17

3. Particle - associated aspirationParticle-associated aspiration is defined as the inhalation of particulate matter of

gastric contents, resulting in an acute obstruction of smaller and possibly also largerairways with the consequence of sudden arterial hypoxemia and the development ofatelectases distal to the foreign body.

INCIDENCE AND RISK FACTORS

The occurrence of pulmonary aspiration in the process of the patients perioperativecare belongs to one of the most feared anaesthesia-associated incidents for mostanaesthesiologists. According to Webb et al., aspiration and regurgitation are ranked

the fifth most common adverse event which can occur during general anaesthesia.25

The risk of aspiration has been examined in several studies in different countries inthe past.26e36 However, the methodology of the individual studies is very differentwith partial retrospective, partial prospective designs. Secondly, the definitions for

Table 1. Contrasting features of aspiration pneumonitis and aspiration pneumonia (Copyright 2001

Massachusetts Medical Society17).

Feature Aspiration pneumonitis Aspiration pneumonia

Mechanism Aspiration of sterile

gastric contents

Aspiration of colonized

oropharyngeal materialPathophysiologic

process

Acute lung injury from acidic

and particulate gastric

material

Acute pulmonary inflammatory

response to bacteria and bacterial

products

Bacteriologic

findings

Initially sterile, with subsequent

bacterial infection possible

Gram-positive cocci, gram-negative

rods, and (rarely) anaerobic bacteria

Chief

predisposing

factors

Markedly depressed level of

consciousness

Dysphagia and gastric dysmotility

Age group

affected

Any age group, but

usually young persons

Usually elderly persons

Aspiration

event

May be witnessed Usually not witnessed

Typical

presentation

Patient with a history of a

depressed level of consciousness

in whom a pulmonary infiltrate

and respiratory symptoms develop

Institutionalized patient with dysphagia

in whom clinical features of pneumonia

and an infiltrate in a dependent

bronchopulmonary segment develop

Clinical features 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

Tachypnoea, cough, and signs of

pneumonia

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the inclusion of an event as perioperative pulmonary aspiration, the criteria of its di-agnosis as well as the clear differentiation between aspiration pneumonitis and aspira-tion pneumonia vary between the individual studies. These factors make it hard tocompare the results from these studies.

Large studies on the incidence of aspiration and its associated mortality in theperianaesthetic 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 oneevent in 2000 to 3000 anaesthesias. Concerning the aspiration incidence in childrencompared with adult patients, there are contradictory data in the literature. Severalstudies suggest that paediatric patients compared to adults have a two- to three-foldhigher risk of perioperative pulmonary aspiration.26,36 Other prospective long-termstudies did not confirm this increased risk.34,35

Several factors have been identified which are accompanied by an increased risk ofaspiration.37e39 These risk factors predisposing to aspiration are summarized inTable 3. Compared to the incidence with elective procedures, the occurrence of a pul-monary 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 riseswith patients aged over 60. According to Kozlow et al., patients over 80 years haveeven a nine- to tenfold increased risk of aspiration in comparison to the group of18- to 29-year-olds.37

It is generally held that obstetric anaesthetic practice is a high-risk area for aspira-tion and also that the mortality rate is likely to be more frequent during obstetric as-piration than during general surgery.52 Compared to gynaecological patients of similarage, caesarean section patients still have an increased risk of aspiration pneumonitis.53

The decrease in anaesthesia-related maternal death is clearly the result of replacinggeneral 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, stratified by surgi-

cal group, is presented in Table 4. The surgical group that had the highest prevalence ofaspiration pneumonia involved patients undergoing tracheostomy procedures with19.1%, compared with an average of 0.7% in patients undergoing procedures otherthan tracheostomy37, probably because the airway is not protected during the changeof cannule.

In summary, the total risk of an aspiration seems to be small in elective generalsurgical patients undergoing general anaesthesia, with a negligible morbidity and mor-tality.38 Nevertheless, each individual case of aspiration pneumonia, apart from the

consequences for the patient, involves also a substantial economic cost factor. The oc-currence of aspiration pneumonia is on average associated with a 15-day prolongationof the length of stay in hospital, and additional costs amount to about $22,000, asshown 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 re-viewed 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, cri-coid pressure is considered a simply accomplished and effective method for the pre-vention of regurgitation and aspiration of gastric contents.55 This procedure, in whicha possible reflux is to be prevented by compression of the oesophagus between the



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Table 2. Incidence of aspiration.

Reference Country/Period

of assessment

Study size Patient group Incidence

Overall

rate

Em

pro

Retrospective study design

Olsson26 Sweden 1967e1970, 1975e1983 185.358 Children/Adults 1: 2.131 Asp

pro

Hovi-Viander27 Finland 1975 338.934 Children/Adults NR NR

Cohen28 Canada 1975e

1983 112.721 NR 1: 1116 NRWarner29 USA 1985e1991 215.488 Adults 1: 3216 1:89

Prospective study design

Harrison30 South Africa 1967e1976 240.483 NR NR NR

Tiret31 France 1978e1982 198.103 Children/Adults 1: 7.335 1-2

Leigh32 UK 1984e1988 84.835 Children/Adults 1:14.139 NR

Mellin-Olsen33 Norway 1989e1993 85.594 Children/Adults 1: 3.424 1:80

Tiret34 France 1978e1982 40.240 Children 1:10.060 NR

Warner35 USA 1985e1997 63.180 Children 1: 2.632 1:37

Murat36 France 2000e2002 24.165 Children 1: 1.272 NR

(NRNot reported).


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ring cartilage and the cervical vertebral bodies, is generally recognized, although a clin-ical benefit of this wide-spread method in the sense of an outcome improvement couldnot be proven so far in controlled clinical studies. The recommendations regarding theperformance 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 thereare differing opinions about the efficacy and necessity of cricoid pressure at all asa firm component of rapid-sequence induction. The occurrence of complications is

Table 3. Factors indicating an increased risk for aspiration.

Gastric content Increased risk of regurgitation Laryngeal incompetence

Delayed gastric emptying

(traumatized patients,

pyloric spasm, ileus, drugs)

26,35

Reflux oesophagitis35,39 Prehospital intubation46,47

Drugs (opioids, sedatives)39 Geriatric patients37,40 General anaesthesia

- Emergency surgery26,29,31,33,35,39,48

- Night-time surgery26

- Inadequate anaesthesia29,39,49

Gastric hypersecretion

(pain, stress)26Obesity

- Pro26,39,41

- Contra42,43

Diabetic autonomic

neuropathy

-

Pro

44

- Contra45

Hiatus hernia39,63

Head injury/Trauma26

Neuromuscular disorders/

Neurological deficit39,50,51

- Multiple sclerosis

- Parkinsons disease

-

Guillain-Barre- Muscular dystrophies

- Cerebral palsy

Table 4. Incidence of aspiration pneumonia by surgical group for 318,880 adult surgical patients in 52

Maryland hospitals, 1999e2000.37

Surgical group Incidence of aspiration pneumonia, %

Tracheostomies 19.1

Respiratory system 2.1

Nervous system 1.4Integumentary system 1.3

Digestive system 1.1

Nose, mouth, pharynx 1.1

Hemic and lymphatic system 0.9

Cardiovascular system 0.7

Ear 0.7

Urinary system 0.6

Musculoskeletal system 0.5

Male genital system 0.3

Endocrine system 0.2

Eye 0.1Female genital system


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rare when indications and contraindications are considered carefully and when themanoeuvre is performed correctly, particularly regarding the force and the durationof application.

The work of Vanner et al. provided the pathophysiological background for the re-quirement of cricoid pressure. They demonstrated that the upper oesophageal sphinc-ter tone decreased in patients after the induction of intravenous anaesthesia with

thiopental, midazolam and succinylcholine from on average 39 mmHg in awake condi-tion to less than 10 mmHg, permitting the regurgitation of gastric contents into thepharynx.56 On the other hand, it is well-known that cricoid pressure itself degradesthe tone of the lower oesophageal sphincter, probably caused by a pharyngeal re-flex, 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, isthe compression of the oesophagus between the ring cartilage and the cervical ver-tebral bodies to prevent a possible reflux of gastric contents. With the one-handedvariant of this method the thumb and the middle finger are placed on each side ofthe cricoid cartilage (Figure 1). The index finger should be set above the cartilage to

avoid the lateral deviation of the cricoid. Ideally with this procedure a compressionof the upper oesophagus sphincters against the sixth cervical vertebral body is reached.

The Sellick manoeuvre should begin already with application of the intravenousopiate and hypnotic medication, thus before complete loss of consciousness by thepatient, because in this part of anaesthesia induction the sphincter tone already de-creases. 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).

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from an awake value of 43 to 9 mmHg after thiopentone and from 38 to 7 mmHg aftermidazolam application.56 The force exerted with cricoid pressure is generally indicatedin Newton, whereby 9.81 N corresponds to a resting upon weight of 1 kg. Consider-ing that execution of the procedure on the awake patient can cause pain and inducevomiting, the initial force at the time of pre-oxygenation should be restricted to 10N 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 maintainedcontinuously until the completion of intubation including blocking of the tube cuff andconfirmed endotracheal location of the tube. Crucial for the performance of cricoidpressure is the dosing of the force in order to ensure sufficient aspiration protection,on the one hand, and prevent difficulties with laryngoscopy and intubation due to toostrong pressure, on the other.

The most limiting feature of cricoid pressure is that it can cause anatomical distor-tion of the upper airway (e.g. pharyngeal compression, distortion/malalignment of thelarynx/trachea, activation of upper airway reflexes), making airway management moredifficult.60 Incorrect application of the manoeuvre may deform the cricoid cartilage,

close vocal cords and impair ventilation, especially in female patients.61 Excessiveforce, wrong (lateral) direction of the force or application of pressure on the larynxrather than on the cricoid ring would make visualization of the larynx and intubationdifficult or impossible. On the other hand, cricoid pressure applied correctly bytrained personnel does not increase the rate of failed intubation.62

The procedure of cricoid pressure is affirmed with appropriate indication as a pre-ventive method in principle also by paediatric anaesthesiologists63, although the inci-dence of mechanical airway obstruction is increased due to cricoid pressure straightin infancy.64

Active vomiting leads to a retrograde peristaltic wave, which can lead to an oesopha-

geal rupture when cricoid pressure is maintained. For this reason, cricoid pressureshould be released immediately and the head-down position (anti-Trendelenburg posi-tion) reverted when active vomiting occurs. Nevertheless, there have been discussionsrecently as to whether this is justifiable in view of the risk of a possible aspiration.65

When the contraindications for the application of cricoid pressure, such as activevomiting, difficult airway conditions, and injuries to the larynx, are considered, seriouscomplications are rare.60 A case report indicates that oesophageal rupture may occurin rapid-sequence induction of anaesthesia for surgery of haematemesis due to a bleed-ing gastric ulcer.66 This may be due to rapidly increased pressure during vomiting thatrupture 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 thata rupture of the oesophagus occurred in 3 out of 10 cases when cricoid pressurewas performed with a force of 30 to 40 N. On the other hand, they showed thatwith a pressure of 20 N, a strength maximally tolerated by an awake patient, no oeso-phageal 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 ofcricoid pressure application are rather unsatisfactory under anaesthesiologists and an-aesthesia personnel.69e72 Forty per cent of anaesthesiologists in southern Sweden werenot aware of possible contraindications to cricoid pressure, and 69% had never heard offorce conditions which can be exerted during the cricoid pressure procedure.72 A sim-

ilar picture emerged under obstetrical anaesthesiologists in France, half ofwhom werenot able to describe the technology of applying cricoid pressure correctly.69

According to available data, it is doubtful whether cricoid pressure is always cor-rectly accomplished in practice, regarding its execution, the force employment and



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the temporal operational sequence during the rapid-sequence induction. Under thecriterion of rising complications due to inaccurate performance, i.e., with an increaseof risk instead of usefulness as a consequence of ineffective application, it is necessaryto train medical and nursing personnel on a regular and purposeful basis as aprecondition for correct application of cricoid pressure. On the other hand, thiscould 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 thepatient.

TREATMENT OF ASPIRATION

Principles of crisis management

The management of critical events is one of the most challenging and important tasksan anaesthesiologist can face in clinical practice. For successful incident management in

anaesthesia, dynamic decision-making with the application of prepared algorithms isnecessary. According to Gaba et al.73, the basic principles of medical crisis managementare based on the following components:

Observation

Clinical observation of the patient using the monitoring available as well as verificationof 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 theassigned procedures.

Recalling such a structural procedure should be the basis of managing an acute pul-monary aspiration arising during general anaesthesia. Kluger et al. showed that thecorrect application of an explicit algorithm during the occurrence of aspiration l edto earlier recognition and/or to better management of the problem in 19% of cases.74

Practical procedure

The first step for the successful management of an aspiration is immediate recognitionof 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

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- 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 defined first against similar differential-diagnostical events (decisions). Bron-chospasm, pulmonary edema, ARDS, pulmonary embolism, and obstruction of the en-dotracheal tube can produce a similar respiratory picture as aspiration. In a study fromAustralia, the diagnosis of regurgitation, vomiting, and aspiration was confirmed byclinical observation in 70% of 183 relevant incidents among 4000 reports, whereasin 15% of the cases aspiration occurred primarily as an unexplained decrease in satu-ration, in 6% as laryngospasm, in 3% as obstruction of the airway, in 2% as broncho-spasm and in 1% with hyperventilation, while 1% were accompanied by a difficultintubation, and 0.5% of the cases occurred with pulmonary edema as well as cardiacarrest.74

If the diagnosis of aspiration is suspected, the following procedures should be doneand adapted to the situation (to act). If a pulmonary aspiration was already recognizedduring induction of anaesthesia and/or during laryngoscopy, immediate endotrachealsuctioning is indicated, followed by an immediate orotracheal intubation in form ofa rapid-sequence induction. Each of the following manoeuvres should be performedconsidering the following principle: no unnecessary time may be lost with respectto a possibly dropping oxygen saturation of the patient. Highest priority in this situa-tion is the maintenance of an adequate oxygenation of the patient.

For this, a controlled ventilation with an inspiratory oxygen fraction of 1.0 shouldbe accomplished and a positive endexpiratory airway pressure (PEEP) should be in-

stalled at least at about 5 cmH2O.75In case aspiration occurs after completing the intubation, the patient should be

brought immediately into a head-down position. An endotracheal suctioning by thetube using a large suction catheter is indicated. A lavage over the tube is usually notindicated after the aspiration of liquids, for example of pure gastric acid, since bythis procedure a distribution of the aspirate into deeper, peripheral lung sectionscan be provoked.

If the aspiration of particulated matter is assumed, a bronchoscopy should be per-formed. The careful elimination of all particles with flexible fibre optics is recommen-ded, while samples of the lung aspirates should be taken for determination of the pH as

well as for a microbiological diagnosis. Larger firm particles must in any case be re-moved by bronchoscopy in order to prevent the development of airway obstructionwith 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 ap-plication of a systemic (theophylline) or topical (salbutamol) bronchodilator can be help-ful for the dilatation of larger, spastic airways in less damaged lung areas which areconstricted due to a reflex mechanism. However, the use of the bronchodilatory effectof inhalation anaesthetics should be avoided after an acid-associated aspiration in thecontext of a general anaesthesia, since there are data suggesting a reinforcement of

acute inflammatory reaction e.g. by isoflurane, enflurane, and halothane.76

A sufficient fluid management is essential as accompanying therapy, since volumeshifts with consecutive haemodynamic changes may occur following a developingpulmonary edema.



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After successful management of the initial phase following pulmonary aspiration,the progress of the planned operation has to be discussed in consent with the surgicalcolleagues. Here elective surgery should be cancelled wherever possible and emer-gency surgery should be limited to the smallest procedure which is compatible withthe patients security.

Each action should be accompanied by tight control of the situation and the ques-

tion should be asked as to whether the condition of the patient has improved orwhether further actions are required (re-evaluation). According to the severity of aspi-ration, frequent arterial blood gas analyses should be performed in order to optimizemechanical ventilation by adjusting the inspiratory oxygen concentration, the respira-tory rate, and the PEEP level.

A chest X-ray should be done as soon as possible in any case of suspected pulmo-nary aspiration to specify the pulmonary pathology. However, it must be pointed outthat in approximately 25% of cases radiographic signs of an aspiration are missinginitially.

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 aretrospective study that such patients neither showed respiratory consequences laternor required further postoperative interventions.29 Patients who are stable afterextubation during a period of two hours in the recovery room (oxygen saturationat least 95% under an FiO2< 0.5, heart rate


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Nevertheless, antibiotics are nowadays often applied before the isolation of germs,although larger controlled studies of empirical or calculated antibiotic therapy in thecontext of pulmonary aspiration have not been done. A national survey in the UnitedStates of America performed in 2001 confirmed this procedure. 51.9% of physiciansstarted administering antibiotics already at the suspicion of an aspiration, and 77.7%with confirmed aspiration before definite proof of an infection. In the context of

the treatment of definite aspiration pneumonia, 27.6% of physicians preferred a path-ogen specific therapy, whereas 72.4% chose the antibiotic empirically.24

If the initiation of an antibiotic therapy seems to be necessary due to the clinicalprogress before the proof of a germ, the choice of the antibiotic therapy should bebased on the clinical condition of the patient and on the typical spectrum suspectedin aspiration pneumonia acquired in the particular hospital. Penicillin and clindamycinare frequently used as first-line antibiotics for the empirical treatment of aspirationpneumonia 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 seemequally effective.84,85 Due to the fact that anaerobes possibly no longer take the pre-dominant place in the spectrum of the pathogenic germs, a change in the antibioticstrategy seems to be indicated.23 Antibiotics with effectiveness against gram-negativebacteria, like third-generation cephalosporins or fluoroquinolones, gain importance inthis context.17

However, structured clinical pathways that account for the cost-effectiveness ofdelaying initial antimicrobial therapy until an aspiration diagnosis is documented, alongwith 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 placein the management of pulmonary aspiration. A reduction and/or inhibition of the in-flammatory reaction in the acute phase by application of high-dose corticoidsteroids has not been confirmed in these patients.86e92 On the contrary, the useof steroids can even have an unfavourable effect on the mortality of critically illpatients.86,87 Hence, corticosteroids should not be given prophylactically in the acutephase of aspiration.81

Altogether the management of pulmonary aspiration is nonspecific and adjuvant.Future research work should focus on the development of intratracheally12 or in-travenously applicable drugs for the neutralization of the effects caused by the as-piration of particulate matter, particularly with low pH values. Until today, aneffective pharmacological therapy for patients after acid aspiration has not been es-tablished despite its enormous clinical relevance due to the mortality of aspirationpneumonitis.17 Animal studies have shown some promising results. The early appli-cation of the phosphodiesterase inhibitor pentoxifylline improved oxygenation byreducing the release of the proinflammatory cytokine TNF -a in rats. Additionally,pentoxifylline significantly increased survival rate probably due to its additional ino-

tropic effect.93

Also the application of thymoquinon, an extract from black cumin(Nigella sativa) with anti-inflammatory, bronchodilatory and antibacterial effects,provided better oxygenation as well as histopathologically smaller damage to thelung tissue in the rat.94



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SUMMARY

The aspiration of gastric contents can cause a broad spectrum of symptoms and clinicaloutcomes, ranging from mild asymptomatic and in themselves limited episodes up tothe development of a severe pneumonitis with transition to an acute respiratory dis-tress syndrome (ARDS). For the management of pulmonary aspiration, differentiationbetween aspiration pneumonitis and aspiration pneumonia is of crucial importance.

The incidence of aspiration during elective surgery amounts to 1 per 2000e3000anaesthesias for adults and 1 per 1200e2600 anaesthesias in children. In emergencysurgery the incidence is three to four times higher. The risk is particularly increasedin 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, rapid-sequence-induction techniques are used, which are clinically common and widelyaccepted, although their use has not been confirmed in the sense of an outcomeimprovement for the patients. Future studies should aim at the evaluation of manoeu-vres like the optimal position of the patient during rapid-sequence induction or theefficacy of cricoid pressure.

The therapy of confirmed aspiration is symptomatic and adjunctive, whereby themain goal is the maintenance of an adequate oxygenation. The application of cortico-steroids and/or antibiotics should be omitted in the acute phase, since there is noevidence of an outcome improvement.

Pulmonary aspiration should be treated using explicit algorithms which have beenshown to accelerate problem recognition and improve therapy. However, furtherresearch is necessary to support this strategy.

Practice points

Algorithm following the Crisis management manual of the Australian PatientSafety 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

422 M. Janda et al


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Research agenda

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Proof of efficiency of different measures/strategies in the course of the rapidsequence induction as for example of the application of the cricoid pressureor different storage techniques (head high and/or head down position)

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