From the *Department of Anesthesia and Critical Care, Airway Study and Training Center, University of Chicago; and †Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Department of Anesthesiology, University of Illinois College of Medicine, Chicago, Illinois.
Accepted for publication June 18, 2009.
Address correspondence and reprint requests to Andranik Ovassapian, MD, Department of Anesthesia and Critical Care, Airway Study and Training Center, University of Chicago, 5841 South Maryland Ave., Chicago, IL 60637. Address e-mail to firstname.lastname@example.org.
The introduction of cricoid pressure (CP) by Sellick1 in 1961 “to control regurgitation until intubation with a cuffed endotracheal tube was completed” was met with an enthusiastic reception worldwide and rapidly became an integral component of the rapid sequence induction/intubation technique (RSII). The maneuver consisted of “occlusion of the upper esophagus by backward pressure on the cricoid ring against the bodies of cervical vertebrae to prevent gastric contents from reaching the pharynx.”1 Sellick1 provided evidence that extension of the neck and application of CP obliterated the esophageal lumen at the level of the 5th cervical vertebra, as seen in a previously placed soft latex tube distended with contrast media to a pressure of 100 cm H2O. He also confirmed the value of CP in preventing saline (run into the esophagus from a height of 100 cm H2O) from reaching the pharynx in a patient undergoing gastroesophagectomy.2 Sellick1,2 emphasized that the lungs can be ventilated by intermittent positive pressure and that CP can prevent inflation of the stomach during positive pressure ventilation. References to CP were found in the literature more than 230 yr ago.3 In a letter from Dr. W. Cullen to Lord Cathcart dated August 8, 1774, concerning the recovery of persons “drowned and seemingly dead,” the use of CP by Dr. Monro was referred to as a means of preventing gastric distension during inflation of the lungs.3
Before Sellick described CP, several techniques were used in patients at risk of aspiration of gastric contents: awake intubation, induced hyperventilation with carbon dioxide during inhaled induction,4 and RSII performed with the patient in a 40° head-up tilt.5 The rationale behind the head-up tilt was that gastric contents could not reach the laryngeal level even if contents were moved up into the esophagus.5 The RSII with CP was extended not only to emergency surgical and obstetrical procedures and the critical care setting, but also to elective procedures in patients at risk of aspiration of gastric contents. The plethora of manuscripts, correspondence, and reviews on CP is a testimony to its relevance to anesthetic practice and continuing interest to clinicians.6
In the last 2 decades, clinicians have questioned the efficacy of CP and therefore the necessity of the maneuver.7,8 Some suggested abandoning it on the following grounds: (a) Its effectiveness has been demonstrated only in cadavers,9–11 and therefore its efficacy lacks scientific validation. (b) It induces relaxation of the lower esophageal sphincter.8,12 (c) There have been reports of regurgitation of gastric contents and aspiration despite CP.13 (d) The esophagus is not exactly posterior to the cricoid, and thus the maneuver is unreliable in producing midline esophageal compression.14 (e) It is associated with nausea/vomiting and also with esophageal rupture.15 (f) It makes tracheal intubation and mask ventilation difficult or impossible.15–18
Because of ethical considerations, a controlled study of the efficacy of CP is not feasible. Even if such a study were conducted, it would probably yield little information, given the low incidence of pulmonary aspiration. The compelling evidence supporting the effectiveness of CP comes from studies that unequivocally demonstrate its efficacy in preventing gastric inflation in anesthetized children and adults.19–21 It is inconceivable that a maneuver effective in preventing gastric inflation during manual ventilation would not be effective in preventing esophageal contents from reaching the pharynx.
The study by Rice et al.22 in the current issue sheds new light on the efficacy of CP. In 24 awake volunteers, magnetic resonance imaging was performed with and without CP in sniffing, neutral, and extended head positions. Without CP, the diameter of the postcricoid hypopharynx was 7.3 ± 1.9 mm. The anteroposterior thickness of the anterolateral wall (2.6 ± 1.0 mm) and posterior wall (3.5 ± 1.2 mm) added up to 6.1 mm. Because the anteroposterior diameter of the postcricoid hypopharynx with CP measured only 4.7 ± 1.4 mm, the authors inferred that the lumen of the alimentary tract posterior to the cricoid cartilage was indeed compressed.22 This finding clearly demonstrates the efficacy of CP. Furthermore, magnetic resonance imaging showed compression of the postcricoid hypopharynx during CP regardless of the position of the cricoid cartilage (midline or lateral displacement) relative to the vertebral body.22
Unlike “the cervical esophagus,” Rice et al.22 observed that the postcricoid hypopharynx moved with the cricoid ring as an anatomic unit, an anatomical relationship that has been described previously.23 Although they distinguished between the postcricoid hypopharynx, the part of the alimentary tract compressed by CP, and the esophagus, they referred to the postcricoid hypopharynx as the “cricopharyngeus.” The question remains: Is the postcricoid hypopharynx a part of the esophagus or a separate entity? Clinicians have regarded the cricopharyngeus as a major component of the upper esophageal sphincter. Its muscle tone creates a sphincteric pressure (mean 38 mm Hg, in awake subjects) that prevents esophageal contents from reaching the pharynx (second line of defense).24 Sphincter pressure increases slightly during inspiration preventing air entry into the esophagus but markedly decreases with neuromuscular blockade.25 Although distinct from the remainder of the cervical esophagus, one can argue that the postcricoid hypopharynx (the cricopharyngeus) is the upper esophagus.
It has been suggested that pulmonary aspiration despite CP may reflect concomitant reflex relaxation of the lower esophageal sphincter,8 which is not attenuated by prior administration of metoclopramide.12 This suggestion is unlikely for several reasons: (a) The purpose of CP is to prevent gastric contents from reaching the pharynx, not to prevent gastroesophageal reflux. (b) In a study of healthy volunteers, gastroesophageal reflux did not occur during CP.26 (c) The incidence of pulmonary aspiration, with the use of a laryngeal mask airway (LMA), which is also known to decrease lower esophageal sphincter tone,27 is not higher than that associated with tracheal intubation.28
Sellick recommended that CP should be applied “lightly” first, then with “firm” pressure exerted when consciousness is lost. Based on studies of cricoid force to prevent material from reaching the pharynx, 40 N (10 N = 1.0 kg) was recommended.29 Studies showed that 34 and 30 N occluded a manometry catheter behind the cricoid cartilage in all patients at a pressure greater than 30 and 25 mm Hg, respectively.24,29 In a cadaver study, 20 N prevented the regurgitation of esophageal fluid at a pressure of 25 mm Hg, and 30 N prevented regurgitation at a pressure of 40 mm Hg.30 Accordingly, the current recommendation is to apply 10 N when a patient is awake, and increase the force to 30 N once the patient loses consciousness.15 Evidence is mounting regarding improper application of CP by anesthesia personnel.30 In one survey, 48% of participants did not apply CP properly. Conversely, anesthesia personnel can be trained to perform the correct maneuver by practicing on weighing scales.31 With proper training, the correct force applied is reproducible within a range of 2 N.31
Cricoid force greater than 40 N can compromise airway patency and cause difficulty with tracheal intubation.6,15,16 CP may displace the esophagus,14 make ventilation with a facemask or with an LMA more difficult,6,17 interfere with LMA placement and advancement of a tracheal tube,6,16,18 and alter laryngeal visualization by a flexible bronchoscope.16 Other investigators have found that CP does not increase the rate of failed intubation.32,33 Releasing CP is certainly justified if the glottic view remains distorted or mask ventilation and tracheal intubation become difficult.
Contrary to Sellick’s recommendations, the current teaching is to avoid manual ventilation of the lungs before intubation during RSII to prevent gastric distension, a potential cause for regurgitation. The effectiveness of CP in preventing gastric insufflation was first recognized in 1974.15 Subsequent studies confirmed that CP prevents gastric distension even when inflation pressures as high as 60 cm H2O are used, provided the airway remains clear.15–17 Thus, manual inflation of the lungs need not be withheld before intubation during RSII. In patients with insufficient oxygen reserve, or when consumption is high or when a nondepolarizing muscle relaxant with a slow onset is used, manual ventilation during CP application is necessary.
CP substitutes for the loss of tone in the cricopharyngeus, nature’s normal defense mechanism. The findings of Rice et al. lend strong support to the efficacy of Sellick’s maneuver in occluding the alimentary tract posterior to the cricoid cartilage. There is strong evidence that gastric insufflation can be prevented by CP, and that mask ventilation can be applied safely during RSII. On the other hand, there are circumstances in which CP or RSII is undesirable or contraindicated. These situations should be respected and other alternative management strategies sought. In the clinical setting, the decision to use CP should be a balance between the potential benefits that have been demonstrated repeatedly, and rare potential complications that are likely a result of improper application of the technique34 but that can easily be taught.31 It is our duty as clinicians to make Sellick’s great contribution a safe practice.
1. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961;2:404–6
2. Sellick BA. The prevention of regurgitation during induction of anaesthesia. In: Proceedings of the First European Congress of Anaesthesiology, Vienna 1962;1:89
3. Salem MR, Sellick BA, Elam JO. The historical background of cricoid pressure in anesthesia and resuscitation. Anesth Analg 1974;53:230–2
4. Inkster JS. The induction of anaesthesia in patients likely to vomit with special reference to intestinal obstruction. Br J Anaesth 1963;35:160–7
5. 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
6. Brimacombe JR, Berry AM. Cricoid pressure. Can J Anaesth 1997;44:414–25
7. Jackson SH. Efficacy and safety of cricoid pressure needs scientific validation. Anesthesiology 1996;84:751–2
8. Tournadre JP, Chessard D, Berrada KR, Boulétreau P. Cricoid cartilage pressure decreases lower esophageal sphincter tone. Anesthesiology 1997;86:7–9
9. Fanning GI. The efficacy of cricoid pressure in preventing regurgitation of gastric contents. Anesthesiology 1970;32:553–5
10. 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
11. Salem MR, Joseph NJ, Heyman HJ, Belani B, Paulissian R, Ferrara TP. Cricoid pressure is effective in obliterating the esophageal lumen in the presence of a nasogastric tube. Anesthesiology 1985;63:443–6
12. Salem MR, Bruringa 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
13. Schwartz DE, Mathhay MA, Cohen NJ. Death and other complications of emergency airway management in critically ill adults. Anesthesiology 1995;82:367–76
14. 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
15. Vanner RG, Pryle BJ. Regurgitation and oesophageal rupture with cricoid pressure: a cadaver study. Anaesthesia 1992;47:732–5
16. Palmer JH, Ball DR. The effect of cricoid pressure on the cricoid cartilage and vocal cords: an endoscopic study in anaesthetized patients. Anaesthesia 2000;55:253–8
17. 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
18. Morgan M. The confidential enquiry into maternal deaths. Anaesthesia 1996;41:689–91
19. 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
20. Moynihan RJ, Brock-Utne J, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insufflation in infants and children. Anesthesiology 1993;78:652–6
21. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric insufflation and rapid sequence induction. Br J Anaesth 1987;59:315–8
22. Rice MJ, Mancusco AA, Gibbs C, Morey TE, Gravenstein N, Deitte LA. Cricoid pressure results in compression of the postcricoid hypopharynx: the esophageal position is irrelevant. Anesth Analg 2009;109:1546–52
23. Tran DO. The correct position of the head and neck for rapid sequence induction. Anesthesiology 1987;67:861
24. Vanner RG, O’Dwayer JP, Pryle BJ, Reynolds F. Upper oesphageal sphincter pressure and the effect of cricoid pressure. Anaesthesia 1992;47:95–100
25. Vanner RG, Pryle BJ, O’Dwyer JP, Reynolds F. Upper oesphageal sphincter pressure and the intravenous induction of anaesthesia. Anaesthesia 1992;47:371–5
26. Skinner HJ, Bedforth NM, Girling KJ, Mahajan RR. Effect of cricoid pressure on gastro-oesophageal reflux in awake subjects. Anaesthesia 1999;54:798–800
27. Rabey PG, Murphy PJ, Langton JA, Barker P, Rowbotham DJ. Effect of the laryngeal mask airway on lower oesophageal sphincter pressure in patients during general anaesthesia. Br J Anaesth 1992;69:346–8
28. Brimacombe JR, Berry A. The incidence of aspiration associated with the laryngeal mask airway: a meta-analysis of published literature. J Clin Anesth 1995;7:297–305
29. Wraight WJ, Chamney AR, Howells TH. The determination of an effective cricoid pressure. Anaesthesia 1983;38:461–6
30. Vanner RG, Asai T. Safe use of cricoid pressure. Anaesthesia 1999;54:1–3
31. Herman NL, Carter B, Van Decar TK. Cricoid pressure: teaching the recommended level. Anesth Analg 1996;83:859–63
32. Turgeon AF, Nicole PC, Trepanier CA, Marcoux S, Lessard MR. Cricoid pressure does not increase the rate of failed intubation by direct laryngoscopy in adults. Anesthesiology 2005;102:315–9
33. McNelis U, Syndercombe A, Harper I, Duggan J. The effect of cricoid pressure on intubation facilitated by the gum elastic bougie. Anaesthesia 2007;62:456–9
34. Selick BA. Rupture of the esophagus following cricoid pressure? Anaesthesia 1982;37:213–4