Rapid sequence induction and intubation (RSII) and awake tracheal intubation are commonly chosen anesthetic techniques for the management of patients at risk of aspiration of gastric or esophageal contents. Because of the associated pathological condition, some of these patients may have a gastric tube (GT), usually a nasogastric tube (NGT), placed preoperatively. There are no clinical guidelines regarding which patient should have a GT placed before anesthetic induction. Furthermore, clinicians are not in agreement whether to keep the GT in situ, withdraw it to the esophagus, or remove it completely before induction of anesthesia.1–3 Surveys and several reviews related to RSII have not addressed issues related to GTs.4–7 We used PubMed/MEDLINE to search the English literature up to September 2012 for articles containing the following key words: “gastric tubes” and “anesthetic induction”; “gastric tubes” and “general anesthesia”; “gastric tubes” and “rapid sequence induction”; “pulmonary aspiration” and “anesthetic induction.” We could not find any randomized clinical trials that addressed the questions of when GT placement should be performed or how to manage a previously placed GT during anesthetic induction. There were 3 prospective clinical trials that investigated the incidence of gastroesophageal (GE) reflux with GTs in trauma patients undergoing general anesthesia,8 in volunteers,9 and in patients undergoing elective abdominal laparotomy.10
This review will discuss the history of GTs and their use during induction of anesthesia in patients at risk of pulmonary aspiration. Given the paucity of hard clinical data, some literature discussed and recommendations made in this review are based on various authors’ clinical experiences. On the basis of available information, an algorithm for the airway management in patients at risk of aspiration due to the presence of esophageal lesions, GE reflux, or gastric distension will be presented to aid in decision making regarding the use of a GT. The Discussion will also address special situations in pediatric patients.
The first account of placement of a GT in humans is credited to Aquapendente in the 17th century, who used a silver tube for the sole purpose of feeding. Other sources contend that it was Hunter in the 1790s who successfully fed a patient via a hollow leather tube made of eel skin that had been stretched over whale bone.11–14 The use of a tube as a “stomach pump” for washing out stomach contents of poisoned patients was described in the 1800s. In 1921, the Levin single-lumen rubber tube was introduced for gastric decompression and feeding. In 1934, Miller and Abbott introduced an extended balloon-tipped intestinal 2-lumen tube, with one tube having a rubber balloon at its tip and the other tube with holes near its tip.11–14 The problems associated with the use of rubber tubes, including difficulty in insertion, frequent obstruction, and allergy, eventually led to the development of tubes made of plastic in the 1950s, first polyethylene, then polyvinyl and silicone, and finally polyurethane. The Salem-Sump tube introduced in the 1960s is a 2-lumen tube: a drainage lumen and a smaller secondary lumen that is open to the atmosphere to allow air to be drawn into the stomach and prevent the suction seal effect on gastric mucosa during suctioning.11–14
A vast array of GTs are currently available with different lengths, sizes, pliability, and special purposes. The radiopaque marker offers the advantage of radiographic localization. Typically, sizes 14 to 20 F are used in adults, whereas smaller sizes are used in infants and children. Large sizes are available for special uses. For example, laparoscopic gastric plication or its modifications, for the surgical treatment of morbid obesity, require the placement of a large GT or a bougie. Sizes varying between 32 and 36 F are used for this purpose.15
The route of insertion of the GT, nasal or oral, depends on many factors. These include whether its use is limited to the intraoperative period or extends to the pre- and postoperative periods; whether the patient is alert or unconscious, whether the patient is tracheally intubated before GT insertion, or whether there is nasopharyngeal pathology or trauma.11–16 The route chosen for the GT placement also depends on the size selected, and the relative risks associated with each route.
The indications for the placement of GTs are in 2 categories: diagnostic and therapeutic. Diagnostic indications include: detecting gastrointestinal (GI) hemorrhage, testing for ingested toxins, obtaining culture specimens, measuring gastric pH and volume, monitoring drainage, and identifying esophagus, stomach, and associated pathology on a chest radiograph.11–16 Therapeutic uses include: feeding, drug administration, lavage of hemorrhage, treatment of hypothermia, and evacuation of contents after drug overdose. GTs are commonly placed to remove gastric and esophageal contents, reduce the risk of aspiration, decrease postoperative vomiting, prevent and treat postoperative gastric dilation and paralytic ileus, relieve symptoms of bowel obstruction, avoid stomach injury during laparoscopy, and improve ventilation.11–18
With the development of the laryngeal mask airway (LMA), the problem of malpositioning of the LMA cuff became recognized. Some newer types of LMAs incorporate a gastric port to separate the respiratory from the GI tract. Successful placement of a well-lubricated GT (up to 16 F) via the gastric port to the stomach accomplishes 2 functions: gastric access, and more importantly, facilitation of proper LMA positioning.19
Because it was believed that gastric distension can lead to pulmonary aspiration, anastomotic leak after GI procedures, and wound dehiscence, it has been common practice since the 1930s to decompress the stomach in patients undergoing abdominal surgery.10 William W. Mayo once wrote “it is more important for a surgeon to carry a nasogastric tube than a stethoscope in his pocket”!20 Some studies supported the routine use of GTs for abdominal and other surgeries. A meta-analysis revealed more frequent abdominal distension and vomiting in patients without GTs.21 Another randomized controlled trial found that the prevalence of vomiting was reduced after cardiac surgery in patients who had GTs as compared with patients without GTs (10% vs 24%).22 Conversely, 1 study suggested that early GT removal after cystectomy with urinary diversion is not correlated with the occurrence of ileus.23 There has been concern that GTs can cause GE reflux. Some studies showed that GTs have no effect,9 whereas others showed a decrease8 or an increase.10
With the common use of GTs, a plethora of complications emerged, varying in degrees from mild to severe.12,13,20,24,25 Severe complications include: coughing and vomiting resulting in undesirable hemodynamic responses and pulmonary aspiration; knotting the GT around itself or around the endotracheal tube (ETT) or epiglottis, causing airway obstruction; tracheobronchial placement leading to severe hypoxemia; airway, esophageal, gastric, pulmonary and mediastinal bleeding, ulcerations, and perforations; intracranial and middle ear placement; and injuries to ophthalmic arteries. Because of these adverse effects, the decision to place a GT in abdominal cases should be made on a selective rather than routine basis.10,26,27 It is beyond the scope of this review to provide a comprehensive discussion of the various uses of GTs (and esophageal bougies) and the complications arising from their use. The reader is referred to alternate sources that address these topics.
Before Sellick described the cricoid pressure (CP) maneuver in 1961,28 several techniques were used to minimize the potential for pulmonary aspiration of esophageal and gastric contents, such as:29–36 regional (and spinal) anesthesia; awake tracheal intubation; induced hyperventilation; IV induction of anesthesia (thiopental) followed by or combined with a muscle relaxant, while the patient was positioned in a 40° head-up tilt. Each of these techniques had its advantages and drawbacks. The use of high spinal anesthesia did not prevent pulmonary aspiration, especially in heavily sedated patients.29,30,33,34 This risk was further enhanced by the increased gastric motility induced by sympathetic block.29,30,33,34 Furthermore, hypoventilation occasionally occurred, requiring assisted ventilation.
Both “awake” oral tracheal intubation, by direct laryngoscopy and “awake” blind nasal intubation were commonly practiced in patients at risk of aspiration.30,31 Tracheal intubation was performed after topical anesthesia or nerve blocks, while the patient was breathing spontaneously.30–32 The rationale for induced hyperventilation during inhaled induction was to prevent breath-holding, a prerequisite for active vomiting.33,34 In this technique, hyperventilation was provoked early and rapidly with carbon dioxide, unconsciousness was quickly obtained, and intubation was performed in an unhurried manner, while spontaneous breathing was preserved.33,34 It was also believed that the antireflux mechanism at the GE junction was intensified with deep inspiration.33,34
The basis for IV induction of anesthesia combined with the use of a muscle relaxant in the head-up tilt “or sitting position” was the finding that the maximal intragastric pressure (IGP) in an anesthetized and paralyzed individual is 18 cm H2O.37,a Because positioning an average-height adult patient in a 40° head-up tilt raises the larynx 19 cm above the GE junction1,29,35–38 (Fig. 1), it was theorized that in this position, gastric contents could not reach the laryngeal level, even if the contents were forced into the esophagus.1,29,35–38 This technique, described by Morton and Wylie in 195135 and by Snow and Nunn in 1959,36 differed only slightly from the currently used RSII in that the head-up tilt (or foot-down tilt) was used instead of CP.
Delaying surgery, removal of gastric contents by a wide-bore GT, and the use of emetics such as apomorphine before anesthetic induction, were all practiced at that time.29 Because of its side effects, the use of apomorphine was quickly abandoned. It was realized that in cases of GI obstruction, the stomach may continue to fill, having once been emptied, and it was necessary to ensure that removal of gastric contents continued up to and during anesthetic induction.28,29,33–36 The use of GTs was common in patients likely to have a distended stomach.33–36 In fact, the lack of complications from vomiting and regurgitation in the series reported by Hodges and Tunstall,39 and Snow and Nunn36 was attributed to the use of GTs. The GTs were kept in place during anesthetic induction. Preoperative placement of a GT was done routinely for surgical emergencies but was not considered acceptable for women in labor.28,33,36,39
Investigators attempted to prevent regurgitation by using a cuffed GT and inflating the cuff at the GE junction.40,41 However, this technique was found to be unsafe because of the difficulty in maintaining a reasonable seal by inflating the cuff without producing esophageal damage.1,40,41 When vomiting occurred, the increase in the esophageal diameter rendered the seal less efficient and the cuff became dislodged.1,40,41 A newly improved GT with an inflatable balloon to occlude the cardia was introduced.42 Despite the inventor’s enthusiasm, the use of the device never gained popularity.
The Cricoid Pressure Maneuver
In 1961, Sellick introduced CP “to control regurgitation of gastric or esophageal contents until intubation with a cuffed endotracheal tube was completed.”28 The maneuver consisted of “occlusion of the upper esophagus by backward pressure on the cricoid cartilage (CC).” He demonstrated that CP obliterated the esophageal lumen at the level of the 5th cervical vertebra after the lumen had been distended by soft latex tubing filled with contrast medium to a pressure of 100 cm H2O.28
Because Sellick’s maneuver was designed for patients at risk of aspiration, many of his patients had NGTs placed before anesthetic induction. Sellick stressed that “all reasonable steps should be taken to empty the stomach and esophagus before anesthesia is induced, but it is dangerous to assume that the stomach can be completely emptied by means of the Ryle’s tube (NGT).”28 In his first publication, he wrote “after final aspiration, the Ryle’s tube should be withdrawn.” He hypothesized that by “tripping the sphincters at the upper and lower end of the esophagus, a NGT increases the risk of regurgitation, and interferes with the compression of the upper esophagus.” The NGT was then replaced after intubation and the stomach drained before the end of the operation.28 After gaining experience with CP, Sellick modified his view regarding the necessity for withdrawal of the NGT immediately before anesthetic induction.43 In a second publication and in a personal correspondence to 1 of the authors (MRS), he emphasized “the safety of CP in the presence of a NGT,” as had been demonstrated in a patient undergoing esophagogastrectomy.43
Sellick’s maneuver was met with an enthusiastic reception, and rapidly became an integral component of the RSII.1,7,29,44 The new RSII with CP was extended not only to emergency surgical and obstetrical procedures and the critical care setting, but also to elective procedures in adult and pediatric patients at risk of aspiration.1,7,29,44 The wide acceptance of CP was primarily because it had overcome the disadvantages of the head-up tilt.1,28,29,45 First, IGPs higher than 20 cm H2O were observed in patients with gastric distension,46 and in these patients, a 40° head-up tilt did not consistently prevent gastric and esophageal contents from reaching the pharynx. Second, once gastric contents reached the pharynx during head-up tilt, aspiration was likely.1,28,29 Third, head-up tilt was undesirable in hypovolemic patients.28 Fourth, head-up tilt may not be effective in children.1 Because of their short esophagus, the placement of children in a 40° head-up tilt does not raise the larynx sufficiently above the GE junction so as to overcome increases in IGP1 (Fig. 1). Furthermore, resting IGP may be higher in anesthetized children than it is in adults due to the relatively small size of the stomach, encroachment of abdominal organs, excessive air swallowing during crying, and strenuous diaphragmatic activity during spontaneous breathing.1
In the past 2 decades, clinicians have questioned the effectiveness of CP and therefore its necessity.47–51 A few suggested abandoning the maneuver on the following grounds: (a) Its effectiveness has been demonstrated mostly in cadavers52–54 and therefore the maneuver lacks scientific validation;47 (b) because the esophagus is not exactly posterior to the CC, CP is unreliable in producing midline upper esophageal compression;55 (c) CP induces reflex relaxation of the lower esophageal sphincter (LES);56,57 (d) there have been reports of pulmonary aspiration despite the application of CP;58 (e) CP can initiate nausea and vomiting, and although very rare, esophageal rupture was reported;45,59 and (f) it can make tracheal intubation, mask ventilation, and LMA placement difficult or impossible.60–64
In his original studies, Sellick used soft latex tubes, which required only slight pressure to be occluded,28 whereas in later studies NGTs made of polyvinyl chloride were used.53,54 Polyvinyl chloride NGTs are too firm to be occluded by CP (Fig. 2). Studies in infant and adult cadavers demonstrated the effectiveness of CP in sealing the esophagus around the NGT.53,54 These findings suggest that an NGT need not be removed before anesthetic induction. If a sudden increase in IGP occurs, the open NGT allows release of gastric contents, while CP prevents these contents from reaching the pharynx.
In 1993, Vanner and Pryle65 shed new light on the effectiveness of CP in the presence of an NGT. They hypothesized that a 30 N force applied to the CC should provide a pressure in excess of 200 mm Hg below the 10 cm2 area of the lamina of the CC (30,000 N/m2 = 30 kPa). However, in practice they found that a 30 N force allows regurgitation of esophageal fluid at a pressure exceeding 40 mm Hg.59 This is because the pressure generated posterior to the CC is not evenly distributed, with some parts only receiving 40 mm Hg pressure.
The anatomy of the area where CP is applied may provide an explanation for this finding. Figure 3 shows computerized tomographic scans at the level of the CC of a male subject with an NGT (filled with contrast) in place first without CP (Fig. 3A) and then with CP (Fig. 3B). When the 2 convex structures of the CC and the cervical body are pressed together, only a part of the alimentary tract lumen can be compressed between them. Slight lateral movement of the CC occurs, which allows the rest of the lumen to be pressed against the longus colli muscle on the side of the vertebral body. The NGT is squeezed sideways to occupy that part of the lumen that is relatively less compressed. These observations suggest that the presence of an NGT does not interfere with compression of the upper esophagus during CP and may actually improve it. In a cadaver study, using measured values of cricoid force, the same authors found that the presence of an NGT increases, rather than decreases, the efficacy of CP.59
Despite the aforementioned evidence supporting the effectiveness of CP in occluding the esophagus around the NGT, Sellick’s early view on the withdrawal of the NGT has been perpetuated by some investigators. In 1991, removal of the NGT before induction was recommended on the basis that the “presence of a NGT disrupts the esophageal sphincters, and serves as a wick for regurgitation.”2 In their recommendations relating to the use of CP during RSII, Brimacombe and Berry,3 in 1997, proposed the withdrawal of the NGT into the esophagus, aspirating the NGT, and leaving it open to air. This suggestion was apparently based on the assumption that the presence of the NGT interferes with the competency of the LES.
AIRWAY MANAGEMENT IN PATIENTS AT RISK OF ASPIRATION AND ROLE OF GASTRIC TUBES: CURRENT CONCEPTS
The anesthetic induction technique depends on many factors including: operative procedure; type and severity of the esophageal or GI pathology; state of consciousness; potential for difficult intubation and difficult mask ventilation; whether the NGT is in place; associated medical conditions; the presence of possible contraindications to the use of RSII or CP.1,7,29,33,34,44,66 On the basis of available information, we propose an algorithm for the airway management in patients with esophageal lesions, GE reflux, and gastric distension (Fig. 4). In the algorithm, guidelines for the use of GTs are also addressed.
Maximal oxygen administration before anesthetic induction is essential in patients at risk of aspiration.67 In most patients, tidal volume breathing for 3 minutes or deep breathing for 1.5 minutes is effective in achieving maximal oxygenation. The presence of an NGT can cause leaks between the face mask and the patient’s face, resulting in air entrainment and lower inspired oxygen concentration,67 which may not be fully compensated for by increasing the fresh gas flow or the duration of oxygen administration. The end point of maximal oxygen administration is an end-tidal oxygen concentration ≥90%.67 In patients who are difficult to intubate or ventilate, pharyngeal oxygen insufflation (or tracheal, in case of upper airway obstruction) after oxygen administration may provide at least an additional 10 minutes of adequate oxygenation during apnea for laryngoscopy and tracheal intubation.67 This apneic mass movement oxygenation can be accomplished through a nasopharyngeal or oropharyngeal cannula, via a laryngoscope, or through a needle inserted in the cricothyroid or cricotracheal membrane.67 Mask oxygen administration should also precede awake fiberoptic intubation and be continued via a nasal cannula or a catheter placed in the mouth. Oxygen insufflation at 3 to 5 L/min via the fiberoptic scope working channel has the benefit of delivering oxygen, clearing secretions, and preventing fogging.68 However, this technique should be used cautiously. Squeezing of the fiberoptic scope by airway obstruction can limit the egress of gases and result in barotrauma especially in children with narrow airways.68
In a comatose patient, the trachea may be intubated before the anesthetic is administered. The associated medical conditions may demand the use of prophylactic measures. In hypovolemic subjects, correction of fluid deficits should be accomplished beforehand, if possible.33,34 The induction technique may be tailored to attenuate sympathetically induced hemodynamic effects of tracheal intubation, especially in hypertensive patients.69 When difficulty with tracheal intubation or mask ventilation is anticipated, awake fiberoptic intubation rather than RSII should be planned.2,7,66 In patients with an unstable cervical spine, where neck manipulation may result in further injury, awake fiberoptic intubation should be considered.2 CP may be contraindicated in the following conditions: retropharyngeal abscess (because of the possibility of rupture of the abscess); a foreign body in the upper esophagus; or laryngeal trauma and cervical spine injury. In these situations, head-up tilt may be used instead of CP.1,7,45,48 Studies reported cervical spine movements varying from minimal to significant with CP.70–73 One study questioned the clinical relevance of any movements by retrospectively analyzing patients who had cervical spine injuries, and found no neurologic sequelae.70
Zenker diverticulum is an outpouching of the mucosa, which develops in the weak area (Killian dehiscence) between the thyropharyngeus and cricopharyngeus muscles.74 Compressible swelling develops as the sac enlarges. Regurgitation of material from the pouch may occur during anesthetic induction, intubation, or even after intubation due to seepage of fluid around the tracheal tube cuff during surgical manipulation.75–78 Emptying of the pouch by the patient exerting external pressure before anesthetic induction is encouraged.75–78 The effectiveness of CP depends on the location of the body of the sac in relation to the CC.75 If the sac is small, the body of the pouch will be at the level of the CC; in such a case, CP will compress the body of the pouch, spilling the contents into the pharynx. If the sac is large, the neck of the pouch will be posterior to the CC, and CP will not empty the contents of the pouch into the pharynx.75 Review of the barium swallow is helpful in determining whether CP should be used if RSII is chosen.75
Various anesthetic regimens including regional anesthesia, awake tracheal intubation, and RSII with CP or head-up tilt have been used successfully for surgical repair of the diverticulum.75,78 Deep and superficial cervical plexus blocks without complications have been reported in a series of 58 patients.78 Regardless of the anesthetic choice, straining, gagging, or coughing should be avoided because they may cause external pressure to the pouch and provoke regurgitation.78 The tracheal tube cuff should be immediately inflated so as to prevent seepage of fluid around the cuff. Insertion of a GT should be avoided because it can cause perforation of the diverticulum.75–77 If placement of a GT is necessary, caution must be exercised.
Achalasia is an idiopathic disorder of the esophagus characterized by impaired relaxation of the LES and esophageal aperistalsis resulting in esophageal dilation, and retention of undigested food mixed with air.79 Food particles may remain in the dilated esophagus for many hours or days regardless of the duration of fasting. This can result in regurgitation, aspiration, respiratory infections, upper respiratory obstruction, tracheal compression, and sudden obstruction of the tracheal tube during anesthesia.79–83 Treatments include endoscopic pneumatic dilation of the LES, surgical myomectomy, and botulinum toxin injection.79 Nitrates can cause transient relaxation of the LES and decompression of the esophageal dilation.82 Removal of material from the dilated esophagus by a wide-bore orogastric tube may lead to prompt resolution of symptoms.81 The insertion of a large-bore orogastric tube is advisable before proceeding with the anesthetic, even if it may not be completely effective in removing all food particles.80,81,83 Although we have used RSII in patients with achalasia, awake intubation may be preferable in severe cases.
For pulmonary aspiration to occur, gastric contents must flow to the esophagus (GE reflux), the contents must reach the pharynx (esophagopharyngeal reflux), and the laryngeal reflexes must be obtunded.16,29,84 Two lines of defense prevent gastric contents from reaching the pharynx, the first at the GE junction, and the second at the upper esophageal sphincter (UES).85–91 Normally, the IGP is 10 to 15 cm H2O higher than the esophageal pressure, which is subjected to the negative intrathoracic pressure.84–86 If there were no mechanism to close the lumen between the 2 cavities, GE reflux would readily occur, especially if favored by gravity. Various “antireflux” mechanisms have been proposed, the most important is the tone of the LES, which maintains a pressure higher than the IGP.84–86 It is the difference between the LES pressure and the IGP, “the barrier pressure,” that determines whether regurgitation will occur. An increase in IGP or a decrease in LES tone will facilitate GE reflux.84–86
The IGP can increase secondary to an increase in intraabdominal pressure or when the normal capacity of the stomach (1.0–1.5 L in adults), which is determined by the compliance of the stomach and by the capacity of the abdominal cavity to accommodate the increased volume, is exceeded.16 The tone of the LES is influenced by neural, hormonal, pharmacologic, and pathologic factors.84–87 An increase in IGP (or intraabdominal pressure) is generally accompanied by an increase in LES pressure. This “adaptive” increase in LES tone occurs with increases in abdominal pressures up to 30 cm H2O, and in normal individuals typically occurs with succinylcholine-induced fasciculations.87 Because succinylcholine-induced increases in IGP are accompanied by disproportionate increases in LES pressure, GE reflux normally does not occur.87 However, this phenomenon may be absent in some patients with GE reflux and gastric distension.85 In these situations, a further increase in IGP may promote GE reflux. In patients with symptoms of GE reflux and symptomatic hiatus hernia, dysfunction of the LES results in a lower barrier pressure, allowing flow of gastric contents into the esophagus.85 Pharmacologic approaches to promote gastric emptying, increase barrier pressure, and decrease or neutralize gastric acidity have gained popularity in the preanesthetic management of patients with GE reflux.88,89 The reader is referred to other sources for more information on this subject. The value of routine use of GTs in patients with GE reflux has not been addressed in the literature.
Certain anesthetic complications or maneuvers can induce GE or esophagopharyngeal reflux. Airway obstruction may cause GE reflux by increasing the pleuroperitoneal pressure difference during strong respiratory efforts and by increasing the IGP due to overaction of the diaphragm.1,29,33,34,37 Positive pressure ventilation (in excess of 20 cm H2O) before tracheal intubation may lead to intermittent opening of the UES and LES, resulting in gastric insufflation and a subsequent increase in IGP.1,29,33,34,37 Normally, the UES tone creates a sphincteric pressure of about 38 mm Hg in awake subjects.90,91 This tone is markedly decreased by muscle relaxants and induction drugs, with the exception of ketamine.91 Relaxation of the UES or its mechanical stretching during intubation can facilitate the flow of esophageal contents, if present, to the pharynx.90,91 It has been suggested that CP substitutes for the loss of the UES tone, which accompanies anesthetic induction and muscle relaxation.45,90,91
GI obstruction can be mechanical as in pyloric stenosis or functional as in ileus caused by peritonitis or trauma. Regardless of the cause, GI obstruction ultimately leads to gastric distension, which can cause an increased IGP, GE reflux, and vomiting.1,16,29,33,34 The decision to insert an NGT before anesthetic induction depends on the degree of distension.8,16,92,93 Assessment of the degree of gastric distension and bowel obstruction can be made from the clinical and imaging findings.92,93 Bedside ultrasonographic assessment of the gastric antrum and body can provide quantitative information about the volume of the gastric contents as well as qualitative information regarding its nature (gas, fluid, or solid).92 An estimated volume in excess of 200 to 300 mL in adults suggests the presence of severe distension and serves as an indication for placement of an NGT before anesthetic induction.92,93
Investigators have argued about whether gastric contents can be removed completely with a GT. Some investigators reported that the volume removed via a GT underestimates the true volume of gastric contents.94 Others demonstrated that this method is a very reliable estimate of the total volume of gastric contents.95 Obviously, many factors influence the success of blind gastric emptying.16,94,95 These include size, type, and patency of the GT and its correct placement, position of the patient, use of external abdominal pressure, and consistency of contents. The use of a multiorifice, vented, large (18 F) GT is more effective than the use of a nonvented GT. Multiple distal openings ensure that nearly all gastric pouches are drained. Even if gastric suctioning does not guarantee complete emptying, it reduces the IGP, and the residual volume becomes clinically insignificant as an aspiration risk.95
Many measures have been proposed to facilitate proper GT placement, the application of which depends on whether the patient is awake or anesthetized and whether the GT is inserted nasally or orally.12,13,20,b These measures include selecting the proper size; generous lubrication; encouraging the awake patient to swallow during insertion; neck flexion or anterior displacement of the thyroid cartilage; advancing the GT along the posterior pharyngeal wall using fingers placed in the pharynx, stiffening the GT by chilling, using a stylet or a Fogarty catheter; guiding the GT through an esophageally placed uncuffed ETT; and advancing the GT under direct-vision laryngoscopy with or without the aid of a Magill forceps. Confirmation of proper GT placement is essential.12,13,20,b Radiologic verification is considered the “gold standard”; however, this may not be feasible. Although not as reliable, other approaches have been used. These include visual inspection and pH testing of aspirate; epigastric/left upper quadrant auscultation for a gurgling noise during air insufflation; manual palpation by the surgeon (intraoperatively); confirmation by direct laryngoscopy or fiberoptic bronchoscopy; and absence of carbon dioxide by capnograph (to exclude tracheal placement). Detection of carbon dioxide implies the presence of the unobstructed GT in the airway. In infants and young children, a GT can often be visually observed “rippling” along the inside of the left abdominal wall during insertion.
Attempts should be made to keep the IGP as low as possible until the time of anesthetic induction. The NGT should not be withdrawn and should be connected to suction during induction. Because the use of an NGT does not guarantee removal of all gastric contents, the anesthesiologist should proceed with the contingency that the stomach will not be completely empty.16,21,29,33,34
CONSIDERATIONS IN PEDIATRIC PATIENTS
The principles of airway management in adult patients at risk of aspiration are in large part applicable to the pediatric population. However, in infants, physiologic and anatomic factors as well as the presence of congenital anomalies present unique challenges to the anesthesiologist.1,17,18 Infants typically have a mild form of relaxation of the LES, which can cause GE reflux during the first month of life. But in only 1 in 500 infants does GE reflux persist beyond 6 weeks of age.1,17,18 The usual manifestations are recurrent regurgitation, apneic spells, paroxysmal coughing, reactive airway disease, pneumonia, and failure to thrive.17,18 GE reflux may be present after repair of esophageal atresia and gastrostomy.17,18 It also occurs in children with spastic quadriplegia, brain damage, and trisomy syndrome in which discoordinated breathing and swallowing are present.17,18 GE reflux resulting in aspiration may occur in dyspneic infants, infants with a weak cough reflex, laryngeal malfunction, or vocal cord paralysis.1 Patients who fail medical therapy or who have life-threatening diseases are candidates for esophageal fundoplication.17,18
Mask ventilation before intubation can result in gastric insufflation in infants and children, especially in the presence of airway obstruction or when airway pressure exceeds 20 cm H2O.96–98 Neuromuscular blockade causes paralysis of the UES and facilitates gastric insufflation at lower airway pressures.98 Gastric inflation can impair ventilation, in addition to inducing GE reflux.17,18 Decompression of the stomach after intubation can be achieved with a GT. A lubricated suction catheter may be used instead. In laparoscopic procedures, a GT is placed before cannulation of the abdomen to decompress the abdomen and to avoid gastric perforation.17,18 The GT is usually removed before tracheal extubation.
Anesthetic management of 3 conditions in pediatric patients warrants discussion: congenital pyloric stenosis (CPS), esophageal atresia with tracheoesophageal fistula, and esophageal fundoplication. Since the surgical correction of CPS was attempted in the early 1900s, attention was drawn to the importance of preoperative gastric emptying to remove gastric contents, and barium used to confirm the diagnosis.17,18,99–101 Palpation of the abdomen for the “pyloric tumor” with the stomach empty was also emphasized. Routine gastric emptying and improved anesthetic and surgical techniques virtually eliminated pulmonary complications.17,18,100,101 By the mid 1970s, ultrasonography offered a safer diagnostic tool, and the concern about aspiration of barium has been eliminated. In many centers, laparoscopic surgery has replaced open methods for the treatment of CPS.17,18
In some countries, contrast media are still used to diagnose CPS. If this is done, only water-soluble contrast media should be used, and the stomach should be irrigated multiple times with warm saline while the patient is in the supine, lateral, and prone positions.17,18 A thorough evacuation of stomach contents greatly reduces the chance of regurgitation during anesthetic induction, and the GT should be left in place during the surgical procedure. This allows the surgeon to test the integrity of the pyloric mucosa after pyloromyotomy. A small volume of air is injected through the GT and the surgeon directs the bubble into the duodenum, and then occludes the bowel lumen proximal and distal to the incision. Mucosal perforation is present if air leakage is detected. After carefully emptying the stomach, tracheal intubation can be performed after IV induction, inhaled induction, or while the patient is awake.102,103 There is no evidence that one technique is safer than the other. Inhaled induction is being used in many centers.100 Cook-Sather et al.103 found that awake intubation is not superior to RSII for the management of CPS.
Esophageal atresia with distal tracheoesophageal fistula is, by far, the most common of the congenital esophageal anomalies.104,105 The diagnosis is usually made after birth when a GT (or a suction catheter) cannot be passed into the stomach, but it may be delayed until feeding begins when choking and coughing occur.105 The diagnosis is confirmed when a radiopaque catheter stops into the proximal esophageal segment at a distance of 10 ± 1 cm from the gumline, as seen in a chest film.17,18 A small amount of contrast can be used to outline the proximal esophageal segment. The presence of intestinal air implies a distal tracheoesophageal fistula. Occasionally, massive abdominal distension occurs causing respiratory embarrassment.17,18,104
A GT is kept in place during the surgical procedure to identify the proximal pouch for the surgeon. Tracheal intubation can be performed after inhaled, IV induction, or rarely while the infant is awake.104,105 Some anesthesiologists prefer intubation during spontaneous breathing, while others prefer intubation after muscle relaxation.105 Severe gastric distension can occur after positive pressure ventilation, leading to cardiopulmonary arrest and gastric rupture.104 Two approaches have been used to prevent this complication: positioning of the ETT in relation to the fistula and preoperative gastrostomy under local anesthesia.104 Because the fistula is usually located just proximal to the carina, the ETT is advanced to the right main bronchus and then gradually withdrawn to a position above the carina where bilateral breath sounds can be auscultated.105 Although gastrostomy can prevent gastric distension, it may provide a low-pressure escape route for gas, thereby increasing flow through the fistula, and compromising pulmonary ventilation.105 One strategy to solve this problem is to place a Fogarty balloon catheter through a bronchoscope into the fistula and then to occlude the fistula by inflating the balloon.105 Another strategy is to insert, under fluoroscopic guidance, a Fogarty catheter retrogradely through the gastrostomy into the distal esophagus.106
The objective of the surgical antireflux procedures is to create an intraabdominal segment of esophagus and a physiologic angle of His.17,18,107,108 The fundoplication of Nissen and the partial wrap of Thal-Nissen have been used. The Thal-Nissen partial wrap is more frequently used to avoid the gas bloat syndrome (gastric distension, aerophagia, and inability to belch or vomit).108 Open and laparoscopic approaches have been used.108 Preoperative use of H2 blockers and motility drugs should be continued. These patients may come to the operating room with a GT in place. In children undergoing antireflux procedures, RSII is commonly used.18 After intubation, the anesthesiologist should maintain access to the head so that the NGT and esophageal dilators can be adjusted without dislodging or obstructing the ETT.17 Children who have severe respiratory compromise or neuromuscular disorders may require postoperative ventilatory support.18
Our review of the literature revealed an evolution in the use of GTs in patients at risk of pulmonary aspiration, especially after the introduction of CP into clinical practice. The current consensus is that a GT should not be withdrawn before anesthetic induction. On the basis of available information, we developed an algorithm to serve as a guide for the anesthetic induction and tracheal intubation in patients at risk of aspiration of esophageal and gastric contents. A variety of clinical scenarios were addressed, including Zenker diverticulum, esophageal achalasia, GE reflux, and gastric distension. This algorithm should be viewed as a basic framework, which can be amended and expanded to encompass new information and emerging approaches and strategies with demonstrated clinical effectiveness. Airway management and the use of GTs in the surgical correction of GI anomalies in infants and children are presented.
Name: M. Ramez Salem, MD.
Contribution: This author helped write the manuscript.
Attestation: M. Ramez Salem approved the final manuscript.
Name: Arjang Khorasani, MD.
Contribution: This author helped write the manuscript.
Attestation: Arjang Khorasani approved the final manuscript.
Name: Siavosh Saatee, MD.
Contribution: This author helped write the manuscript.
Attestation: Siavosh Saatee approved the final manuscript.
Name: George J. Crystal, PhD.
Contribution: This author helped write the manuscript.
Attestation: George J. Crystal approved the final manuscript.
Name: Mohammad El-Orbany, MD.
Contribution: This author helped write the manuscript.
Attestation: Mohammad El-Orbany approved the final manuscript.
This manuscript was handled by: Sorin J. Brull, MD, FCARCSI (Hon).
1. Salem MR, Wong AY, Collins VJ. The pediatric patient with a full stomach. Anesthesiology. 1973;39:435–40
2. Benumof JL. Management of the difficult adult airway. With special emphasis on awake tracheal intubation. Anesthesiology. 1991;75:1087–110
3. Brimacombe J, Berry A. Cricoid pressure in chaos. Anaesthesia. 1997;52:924–6
4. Morris J, Cook TM. Rapid sequence induction: a national survey of practice. Anaesthesia. 2001;56:1090–7
5. Stoddart PA, Brennan L, Hatch DJ, Bingham R. Postal survey of paediatric practice and training among consultant anaesthetists in the UK. Br J Anaesth. 1994;73:559–63
6. Koerber JP, Roberts GE, Whitaker R, Thorpe CM. Variation in rapid sequence induction techniques: current practice in Wales. Anaesthesia. 2009;64:54–9
7. EL-Orbany M, Connolly LA. Rapid sequence induction and intubation: current controversy. Anesth Analg. 2010;110:1318–25
8. Satiani B, Bonner JT, Stone HH. Factors influencing intraoperative gastric regurgitation: a prospective random study of nasogastric tube drainage. Arch Surg. 1978;113:721–3
9. Dotson RG, Robinson RG, Pingleton SK. Gastroesophageal reflux with nasogastric tubes. Effect of nasogastric tube size. Am J Respir Crit Care Med. 1994;149:1659–62
10. Manning BJ, Winter DC, McGreal G, Kirwan WO, Redmond HP. Nasogastric intubation causes gastroesophageal reflux in patients undergoing elective laparotomy. Surgery. 2001;130:788–91
11. Paine JR. The history of the invention and development of the stomach and duodenal tubes. Ann Intern Med. 1934;8:752–63
12. Boyes RJ, Kruse JA. Nasogastric and nasoenteric intubation. Crit Care Clin. 1992;8:865–78
13. Davis JWBenumof JL. Nasogastric intubation. Clinical Procedures in Anesthesia and Intensive Care. 1992 Philadelphia J.B. Lippincott Company:823–44
14. Paine LJ, Carlson HA, Wangensreen OH. The postoperative control of distension, nausea, and vomiting. JAMA. 1933;100:1910–7
15. Skrekas G, Antiochos K, Stafyla VK. Laparoscopic gastric greater curvature plication: results and complications in a series of 135 patients. Obes Surg. 2011;21:1657–63
16. Hardy JF. Large volume gastroesophageal reflux: a rationale for risk reduction in the perioperative period. Can J Anaesth. 1988;35:162–73
17. Holl JWGregory GA. Anesthesia for abdominal surgery. Pediatric Anesthesia. 20024th ed Philadelphia Churchill Livingston:567–86
18. Hammer G, Hall S, Davis PMotoyama EK, Davis PJ. Anesthesia for general abdominal, thoracic, urologic, and bariatric surgery. Smith’s Anesthesia for Infants and Children. 20067th ed Philadelphia Mosby Elsevier:685–722
19. Verghese C, Mena G, Ferson DZ, Brain AIJHagberg CA. Laryngeal mask airway. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:443–65
20. Savassi-Rocha PR, Conceicão SA, Ferreira JT, Diniz MT, Campos IC, Fernandes VA, Garavini D, Castro LP. Evaluation of the routine use of the nasogastric tube in digestive operation by a prospective controlled study. Surg Gynecol Obstet. 1992;174:317–20
21. Cheatham ML, Chapman WC, Key SP, Sawyers JL. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy. Ann Surg. 1995;221:469–76
22. Lavi R, Katznelson R, Cheng D, Minkovich L, Klein A, Carroll J, Karski J, Djaiani G. The effect of nasogastric tube application during cardiac surgery on postoperative nausea and vomiting–a randomized trial. J Cardiothorac Vasc Anesth. 2011;25:105–9
23. Park HK, Kwak C, Byun SS, Lee E, Lee SE. Early removal of nasogastric tube after cystectomy with urinary diversion: does postoperative ileus risk increase? Urology. 2005;65:905–8
24. Ozer S, Benumof JL. Oro- and nasogastric tube passage in intubated patients: fiberoptic description of where they go at the laryngeal level and how to make them enter the esophagus. Anesthesiology. 1999;91:137–43
25. Au-Truong X, Lopez G, Joseph NJ, Salem MR. A case of a nasogastric tube knotting around a tracheal tube: detection and management. Anesth Analg. 1999;89:1583–4
26. Argov S, Goldstein I, Barzilai A. Is routine use of the nasogastric tube justified in upper abdominal surgery? Am J Surg. 1980;139:849–50
27. Mellin-Olsen J, Fasting S, Gisvold SE. Routine preoperative gastric emptying is seldom indicated. A study of 85,594 anaesthetics with special focus on aspiration pneumonia. Acta Anaesthesiol Scand. 1996;40:1184–8
28. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet. 1961;2:404–6
29. Salem MR. Anesthetic management of patients with “a full stomach”. A critical review. Anesth Analg. 1970;49:47–55
30. Collins VJCollins VJ. Endotracheal anesthesia: technical considerations. Principles of Anesthesiology. 19762nd ed Philadelphia Lea & Febiger:363–89
31. Magill IW. Blind nasal intubation. Anaesthesia. 1975;30:476–9
32. Bonica JJ. Transtracheal anesthesia for endotracheal intubation. Anesthesiology. 1949;10:736–8
33. Stevens JH. Anaesthetic problems of intestinal obstruction in adults. Br J Anaesth. 1964;36:438–50
34. Inkster JS. The induction of anaesthesia in patients likely to vomit with special reference to intestinal obstruction. Br J Anaesth. 1963;35:160–7
35. Morton HJ, Wylie WD. Anaesthetic deaths due to regurgitation or vomiting. Anaesthesia. 1951;6:190–201
36. Snow RG, Nunn JF. Induction of anaesthesia in the foot-down position for patients with a full stomach. Br J Anaesth. 1959;31:493–7
37. O’ Mullane EJ. Vomiting and regurgitation during anaesthesia. Lancet. 1954;266:1209–12
38. Wylie WD. The use of muscle relaxants at the induction of anaesthesia of patients with a full stomach. Br J Anaesth. 1963;35:168–73
39. Hodges RJ, Tunstall ME. The choice of anaesthesia and its influence on perinatal mortality in caesarean section. (A review of the use of thiopentone and suxamethonium over the ten-year period 1952-1961). Br J Anaesth. 1961;33:572–88
40. Macintosh RR. A cuffed stomach tube. Br Med J. 1951;2:545
41. Bizzarri D, Giuffrida JG. Intubation of the esophagus; its role in preventing aspiration pneumonia and asphyxial death. Am J Surg. 1957;93:329–34
42. Roewer N. Can pulmonary aspiration of gastric contents be prevented by balloon occlusion of the cardia? A study with a new nasogastric tube. Anesth Analg. 1995;80:378–83
43. Sellick BA. The prevention of regurgitation during induction of anesthesia. Proceeding of the First European Congress of Anaesthesiology Vienna. 1962;1:89
44. Stept WJ, Safar P. Rapid induction-intubation for prevention of gastric-content aspiration. Anesth Analg. 1970;49:633–6
45. Ovassapian A, Salem MR. Sellick’s maneuver: to do or not do. Anesth Analg. 2009;109:1360–2
46. La Cour D. Prevention of rise in intragastric pressure due to suxamethonium fasciculations by prior dose of d-tubocurarine. Acta Anaesthesiol Scand. 1970;14:5–15
47. Jackson SH. Efficacy and safety of cricoid pressure needs scientific validation. Anesthesiology. 1996;84:751–2
48. Brimacombe JR, Berry AM. Cricoid pressure. Can J Anaesth. 1997;44:414–25
49. Lerman J. On cricoid pressure: “may the force be with you”. Anesth Analg. 2009;109:1363–6
50. Benhamou D. Cricoid pressure is unnecessary in obstetric general anaesthesia. Proposer. Int J Obstet Anesth. 1995;4:30–1
51. Gobindram A, Clarke S. Cricoid pressure: should we lay off the pressure? Anaesthesia. 2008;63:1258–9
52. Fanning GL. The efficacy of cricoid pressure in preventing regurgitation of gastric contents. Anesthesiology. 1970;32:553–5
53. Salem MR, Wong AY, Fizzotti GF. Efficacy of cricoid pressure in preventing aspiration of gastric contents in paediatric patients. Br J Anaesth. 1972;44:401–4
54. Salem MR, Joseph NJ, Heyman HJ, Belani B, Paulissian R, Ferrara TP. Cricoid compression is effective in obliterating the esophageal lumen in the presence of a nasogastric tube. Anesthesiology. 1985;63:443–6
55. Smith KJ, Dobranowski J, Yip G, Dauphin A, Choi PT. Cricoid pressure displaces the esophagus: an observational study using magnetic resonance imaging. Anesthesiology. 2003;99:60–4
56. Tournadre JP, Chassard D, Berrada KR, Boulétreau P. Cricoid cartilage pressure decreases lower esophageal sphincter tone. Anesthesiology. 1997;86:7–9
57. Salem MR, Bruninga KW, Dodlapatii J, Joseph NJ. Metoclopramide does not attenuate cricoid pressure-induced relaxation of the lower esophageal sphincter in awake volunteers. Anesthesiology. 2008;109:806–10
58. Schwartz DE, Matthay MA, Cohen NH. Death and other complications of emergency airway management in critically ill adults. A prospective investigation of 297 tracheal intubations. Anesthesiology. 1995;82:367–76
59. Vanner RG, Pryle BJ. Regurgitation and oesophageal rupture with cricoid pressure: a cadaver study. Anaesthesia. 1992;47:732–5
60. Shorten GD, Alfille PH, Gliklich RE. Airway obstruction following application of cricoid pressure. J Clin Anesth. 1991;3:403–5
61. Palmer JH, Ball DR. The effect of cricoid pressure on the cricoid cartilage and vocal cords: an endoscopic study in anaesthetised patients. Anaesthesia. 2000;55:263–8
62. Walker RW, Ravi R, Haylett K. Effect of cricoid force on airway calibre in children: a bronchoscopic assessment. Br J Anaesth. 2010;104:71–4
63. Aoyama K, Takenaka I, Sata T, Shigematsu A. Cricoid pressure impedes positioning and ventilation through the laryngeal mask airway. Can J Anaesth. 1996;43:1035–40
64. Morgan M. The confidential enquiry into maternal deaths. Anaesthesia. 1986;41:689–91
65. Vanner RG, Pryle BJ. Nasogastric tubes and cricoid pressure. Anaesthesia. 1993;48:1112–3
66. El-Orbany M, Woehlck HJ. Difficult mask ventilation. Anesth Analg. 2009;109:1870–80
67. Baraka A, Salem MRHagberg CA. Preoxygenation. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:280–97
68. Gil KSL, Diemunsch PAHagberg CA. Fiberoptic and flexible endoscopic aided techniques. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:365–411
69. Joffe AM, Deem SAHagberg CA. Physiologic and pathologic responses to intubation. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:184–98
70. Donaldson WF 3rd, Towers JD, Doctor A, Brand A, Donaldson VP. A methodology to evaluate motion of the unstable spine during intubation techniques. Spine. 1993;18:2020–3
71. Helliwell V, Gabbott DA. The effect of single-handed cricoid pressure on cervical spine movement after applying manual in-line stabilisation—a cadaver study. Resuscitation. 2001;49:53–7
72. Criswell JC, Parr MJ, Nolan JP. Emergency airway management in patients with cervical spine injuries. Anaesthesia. 1994;49:900–3
73. Ellis DY, Harris T, Zideman D. Cricoid pressure in emergency department rapid sequence tracheal intubations: a risk-benefit analysis. Ann Emerg Med. 2007;50:653–65
74. Payne WS, King RM. Pharyngoesophageal (Zenker’s) diverticulum. Surg Clin North Am. 1983;63:815–24
75. Thiagarajah S, Lear E, Keh M. Anesthetic implications of Zenker’s diverticulum. Anesth Analg. 1990;70:109–11
76. Cope R, Spargo P. Anesthesia for Zenker’s diverticulum. Anesth Analg. 1990;71:312
77. Aouad MT, Berzina CE, Baraka AS. Aspiration pneumonia after anesthesia in a patient with a Zenker diverticulum. Anesthesiology. 2000;92:1837–9
78. Adams CF. Regional anesthesia for repair of Zenker’s diverticulum. Anesth Analg. 1990;70:676
79. Payne WS, King RM. Treatment of achalasia of the esophagus. Surg Clin North Am. 1983;63:963–70
80. Creagh-Barry P, Parsons J, Pattison CW. Achalasia and anaesthesia, a case report. Anaesth Intensive Care. 1988;16:371–3
81. Kendall AP, Lin E. Respiratory failure as presentation of achalasia of the oesophagus. Anaesthesia. 1991;46:1039–40
82. Westbrook J. Oesophageal achalasia causing respiratory obstruction. Anaesthesia. 1992;46:1039–40
83. Walton AR. Acute upper airway obstruction due to oesophageal achalasia. Anaesthesia. 2009;64:222–3
84. Cotton BR, Smith G. The lower oesophageal sphincter and anaesthesia. Br J Anaesth. 1984;56:37–46
85. Dent J, Holloway RH, Toouli J, Dodds WJ. Mechanisms of lower oesophageal sphincter incompetence in patients with symptomatic gastrooesophageal reflux. Gut. 1988;29:1020–8
86. Ng A, Smith G. Gastroesophageal reflux and aspiration of gastric contents in anesthetic practice. Anesth Analg. 2001;93:494–513
87. Smith G, Dalling R, Williams TI. Gastro-oesophageal pressure gradient changes produced by induction of anaesthesia and suxamethonium. Br J Anaesth. 1978;50:1137–43
88. Tasch MD, Langeron OHagberg CA. Aspiration prevention and prophylaxis: preoperative considerations. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:265–79
89. Wali A, Munnur UMAHagberg CA. The patient with a full stomach. Benumof’s and Hagberg’s Airway Management. 20133rd ed Philadelphia Elsevier Saunders:705–22
90. Vanner RG, O’Dwyer JP, Pryle BJ, Reynolds F. Upper oesophageal sphincter pressure and the effect of cricoid pressure. Anaesthesia. 1992;47:95–100
91. Vanner RG, Pryle BJ, O’Dwyer JP, Reynolds F. Upper oesophageal sphincter pressure and the intravenous induction of anaesthesia. Anaesthesia. 1992;47:371–5
92. Perlas A, Chan VW, Lupu CM, Mitsakakis N, Hanbidge A. Ultrasound assessment of gastric content and volume. Anesthesiology. 2009;111:82–9
93. Demaret C, David JS, Piriou V. When should a nasogastric tube be inserted before a rapid sequence induction? Look at the x-rays!. Can J Anaesth. 2011;58:662–3
94. Taylor WJ, Barry AW. Measuring gastric contents during general anesthesia: evaluation of blind gastric aspiration. Can J Anaesth. 1989;36:1–4
95. Hardy JF, Plourde G, Lebrun M, Côté C, Dubé S, Lepage Y. Determining gastric contents during general anaesthesia: evaluation of two methods. Can J Anaesth. 1987;34:474–7
96. Ruben H, Knudsen EJ, Carugati G. Gastric inflation in relation to airway pressure. Acta Anaesthesiol Scand. 1961;5:107–14
97. Salem MR, Wong AY, Mani M, Sellick BA. Efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in pediatric patients. Anesthesiology. 1974;40:96–8
98. Moynihan RJ, Brock-Utne JG, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insufflation in infants and children. Anesthesiology. 1993;78:652–6
99. Strauss AA. Clinical Observation on congenital pyloric stenosis, report of 101 cases. JAMA. 1918;71:807–10
100. MacDonald NJ, Fitzpatrick GJ, Moore KP, Wren WS, Keenan M. Anaesthesia for congenital hypertrophic pyloric stenosis. A review of 350 patients. Br J Anaesth. 1987;59:672–7
101. Bissonnette B, Sullivan PJ. Pyloric stenosis. Can J Anaesth. 1991;38:668–76
102. Cook-Sather SD, Tulloch HV, Liacouras CA, Schreiner MS. Gastric fluid volume in infants for pyloromyotomy. Can J Anaesth. 1997;44:278–83
103. Cook-Sather SD, Tulloch HV, Cnaan A, Nicolson SC, Cubina ML, Gallagher PR, Schreiner MS. A comparison of awake versus paralyzed tracheal intubation for infants with pyloric stenosis. Anesth Analg. 1998;86:945–51
104. Salem MR, Wong AY, Lin YH, Firor HV, Bennett EJ. Prevention of gastric distention during anesthesia for newborns with tracheoesophageal fistulas. Anesthesiology. 1973;38:82–3
105. Ulma G, Geiduschek JM, Zimmerman AA, Morray JPGregory GA. Anesthesia for thoracic surgery. Pediatric Anesthesia. 20024th ed Philadelphia Churchill Livingston:423–66
106. Bloch EC, Filston HC. A thin fiberoptic bronchoscope as an aid to occlusion of the fistula in infants with tracheoesophageal fistula. Anesth Analg. 1988;67:791–3
107. Randolph J. Experience with the Nissen fundoplication for correction of gastroesophageal reflux in infants. Ann Surg. 1983;198:579–84
108. Ashcraft KW, Holder TM, Amoury RA. Treatment of gastroesophageal reflux in children by Thal fundoplication. J Thorac Cardiovasc Surg. 1981;82:706–12