Manual of Emergency Airway Management, 3rd Edition

4. Applied Functional Anatomy of the Airway

Michael F. Murphy

There are many salient features of the anatomy and physiology of the airway to consider with respect to airway management maneuvers. This chapter discusses the anatomical features most involved in the act of intubation, the important vascular structures, and the innervation of the upper airway. Chapter 7 builds on these anatomical and functional relationships to describe anesthesia techniques for the airway. Chapter 20 addresses developmental and pediatric anatomical features of the airway.

We consider each anatomical structure in the order in which it appears as we enter the airway: the nose, the mouth, the pharynx, the larynx, and the trachea (Fig. 4-1).

The Nose

The external nose consists of a bony vault, a cartilaginous vault, and a lobule. The bony vault comprises the nasal bones, the frontal processes of the maxillae, and the nasal spine of the frontal bone. The nasal bones are buttressed in the midline by the perpendicular plate of the ethmoid bone that forms part of the bony septum. The cartilaginous vault is formed by the upper lateral cartilages that meet the cartilaginous portion of the septum in the midline. The nasal lobule consists of the tip of the nose, the lower lateral cartilages, the fibrofatty alae that form the lateral margins of the nostril, and the columella. The cavities of each nostril are continuous with the nasopharynx posteriorly.

Important Anatomical Considerations

· Kiesselbach's plexus (Little's area) is a very vascular area located on the anterior aspect of the septum in each nostril. Epistaxis most often originates from this area. During the act of inserting a nasal trumpet or a nasotracheal tube, it is generally recommended that the device be inserted in the nostril such that the leading edge of the bevel (the pointed tip) is away from the septum. The goal is to minimize the chances of trauma and bleeding from this very vascular area. This means that the device is inserted “upside down” in the left nostril and rotated 180 degrees after the tip has proceeded beyond the cartilaginous septum. Although some authors have recommended the opposite (i.e., that the bevel tip approximate the nasal septum to minimize the risk of damage and bleeding from the turbinates), the bevel away from the septum approach makes more sense and is the recommended method.

· The major nasal airway is between the laterally placed inferior turbinate, the septum, and the floor of the nose. The floor of the nose is tilted slightly downward front to back, approximately 10 to 15 degrees. Thus, when a nasal tube, trumpet, or fiberscope is inserted through the nose, it should not be directed upward or even straight back. Instead, it should be directed slightly inferiorly to follow this major channel. Before nasal intubation of an unconscious adult patient, some authorities recommend gently but fully inserting one's gloved and lubricated little finger to ensure patency and to maximally dilate this channel before the insertion of the nasal tube. In addition, placing the endotracheal tube (ETT; preferably an Endotrol tube) in a warm bottle of saline or water softens the tube and attenuates its damaging properties.

· The nasal mucosa is exquisitely sensitive to topically applied vasoconstricting medications such as phenylephrine, epinephrine, oxymetazoline, or cocaine. Cocaine has the added advantage of providing profound topical anesthesia and is the only local anesthetic agent that produces vasoconstriction; the others cause vasodilatation. Shrinking the nasal mucosa with a vasoconstricting agent can increase the caliber of the nasal airway by as much as 50% to 75% and may reduce epistaxis incited by nasotracheal intubation, although there is little evidence to support this claim. Cocaine has been implicated in coronary vasoconstriction when applied to the nasal mucosa, so it should be used with caution in patients with coronary artery disease (see Evidence section at the end of this chapter).

· The nasal cavities are bounded posteriorly by the nasopharynx. The adenoids are located posteriorly in the nasopharynx just above the nasal surface of the soft palate and partially surround a depression in the mucosal membrane where the eustachian tube enters the nasopharynx. During insertion, the nasotracheal tube often enters this depression and resistance is encountered. Continued aggressive insertion can cause the nasotracheal tube to penetrate the mucosa and pass submucosally deep to the naso- and oropharyngeal mucous membrane (Fig. 4-2). Although alarming when one recognizes that this has occurred, no specific treatment is advised, except that withdrawing the tube and trying the opposite nostril is advised. Despite the theoretical risk of infection, there is no literature to suggest that this occurs. Documentation of the complication and communication to the accepting team on admission is mandatory.

· The soft palate rests on the base of the tongue during quiet nasal respiration, sealing the oral cavity anteriorly.

· The contiguity of the paranasal sinuses with the nasal cavity is believed to be responsible for the infections of the paranasal sinuses that may be associated with prolonged nasotracheal intubation. Although this fact has led some physicians to condemn nasotracheal intubation, fear of infection should not deter the emergency physician from considering nasotracheal intubation when indicated. Securing the airway in an emergency takes precedence over possible later infective complications, and in any case, the intubation can always be changed to an oral tube or tracheostomy, if necessary.

· A nasotracheal intubation is relatively contraindicated in patients with basal skull fractures (i.e., when the maxilla is fractured away from its attachment to the base of the skull) because of the risk of penetration into the cranial vault (usually through the cribriform plate) with the ETT. Careful technique avoids this complication: the cribriform plate is located cephalad of the nares, and tube insertion should be directed slightly caudad (see previous discussion). Maxillary fractures (e.g., LeFort fractures) may disrupt the continuity of the nasal cavities and are a relative contraindication to blind nasal intubation. Again, cautious insertion, especially if guided by a fiberscope, can mitigate the risk.

The Mouth

The mouth, or oral cavity, is bounded externally by the lips and is contiguous with the oropharynx posteriorly (Fig. 4-3).

· The tongue is attached to the symphysis of the mandible anteriorly and anterolaterally and the stylohyoid process and hyoid bone posterolaterally and posteriorly, respectively. The posterior limit of the tongue corresponds to the position of the hyoid bone (Fig. 4-1). The clinical relevance of this relationship will become apparent when the 3-3-2 rule is described in Chapter 7.

· The potential spaces in the hollow of the mandible are collectively called the mandibular space, which is subdivided into three potential spaces on either side of the midline sublingual raphe: the submental, submandibular, and sublingual spaces. The tongue is a fluid-filled noncompressible structure. During conventional laryngoscopy, the tongue is ordinarily displaced to the left and into the mandibular space, permitting one to expose the larynx for intubation under direct vision. If the mandibular space is small relative to the size of the tongue (e.g., hypoplastic mandible, lingual edema in angioedema, lingual hematoma), the ability to visualize the larynx may be compromised. Infiltration of the mandibular space by infection (e.g., Ludwig's angina), hematoma, or other lesions may limit the ability to displace the tongue into this space and render orotracheal intubation difficult or impossible.

· Subtle geometric distortions of the oral cavity that limit one's working and viewing space, such as a high arched palate with a narrow oral cavity or buck teeth with an elongated oral cavity, may render orotracheal intubation difficult. Chapter 6 elaborates on these issues.

· Salivary glands continuously secrete saliva, which can defeat attempts at achieving sufficient topical anesthesia of the airway to undertake awake laryngoscopy or other active airway intervention maneuvers in the awake or lightly sedated patient—for example, laryngeal mask airway insertion, lighted stylet intubation, and so on.

· The condyles of the mandible articulate within the temporomandibular joint (TMJ) for the first 30 degrees of mouth opening. Beyond 30 degrees, the condyles translate out of the TMJ anteriorly onto the zygomatic arches. Once translation has occurred, it is possible to employ a jaw thrust maneuver to pull the mandible and tongue forward. This is the most effective method of opening the airway to alleviate obstruction or permit bag-mask ventilation. A jaw thrust to open the airway is not possible unless this translation has occurred (see Chapter 5).

The Pharynx

The pharynx is a U-shaped fibromuscular tube extending from the base of the skull to the lower border of the cricoid cartilage where, at the level of the sixth cervical vertebra, it is continuous with the esophagus. Posteriorly, it rests against the fascia covering the prevertebral muscles and the cervical spine. Anteriorly, it opens into the nasal cavity (the nasopharynx), the mouth (the oropharynx), and the larynx (the laryngo- or hypopharynx).

· The oropharyngeal musculature has a normal tone, like any other skeletal musculature, and this tone serves to keep the upper airway open during quiet respiration. Respiratory distress is associated with pharyngeal muscular activity that attempts to open the airway further. Benzodiazepines and other sedative hypnotic agents may attenuate some of this tone. This explains why even small doses of sedative hypnotic medications (e.g., midazolam) may precipitate total airway obstruction in patients presenting with partial airway obstruction.

· An “awake look” is advocated during the difficult airway algorithm (see Chapter 2). Being able to see the epiglottis or posterior glottic structures employing topical anesthesia and sedation reassures one that at least this much, and probably more, of the airway will be visualized during an intubation attempt following the administration of a neuromuscular blocking drug. In practice, the glottic view is usually improved following neuromuscular blockade. Rarely, however, the loss of pharyngeal muscle tone caused by the neuromuscular blocking agent leads to the cephalad and anterior migration of the larynx worsening the view at direct laryngoscopy. Although uncommon, this tends to occur more often in morbidly obese or late-term pregnancy patients, in whom there may be submucosal edema.

· The glossopharyngeal nerve supplies sensation to the posterior one-third of the tongue, the valleculae, the superior surface of the epiglottis, and most of the posterior pharynx. This nerve is accessible to blockade (topically or by injection) because it runs just deep to the inferior portion of the palatopharyngeus muscle (the posterior tonsillar pillar) (Fig. 4-4).

The Larynx

The larynx extends from its oblique entrance formed by the aryepiglottic folds, the tip of the epiglottis, and the posterior commissure between the arytenoid cartilages (interarytenoid folds) through the vocal cords to the cricoid ring (Fig. 4-5).

· The superior laryngeal branch of the vagus nerve supplies sensation to the undersurface of the epiglottis, all of the larynx to the level of the false vocal cords, and the pyriform recesses posterolateral to either side of the larynx (Fig. 4-5). The nerve enters the region by passing through the thyrohyoid membrane just below the inferior cornu of the hyoid bone (Fig. 4-6). It then divides into a superior and an inferior branch; the superior branch passes submucously through the vallecula, where it is visible to the naked eye, on its way to the larynx; and the inferior branch runs along the medial aspects of the pyriform recesses.

· The larynx is the most heavily innervated sensory structure in the body, followed closely by the carina. Stimulation of the unanesthetized larynx during intubation causes tremendous reflex sympathetic activation. Blood pressure and heart rate may as much as double. This may lead to the elevation of intracranial pressure, particularly in patients with imperfect autoregulation; aggravate or incite myocardial ischemia in patients with underlying coronary artery disease; or incite or aggravate large vessel dissection or rupture (e.g., penetrating injury to a carotid, thoracic aortic dissection, or abdominal aortic rupture).

· The pyramidal arytenoid cartilages sit on the posterior aspect of the larynx (Fig. 4-5). The intrinsic laryngeal muscles cause them to swivel, opening and closing the vocal cords. An ETT that is too large may, over time, compress these structures, causing mucosal and cartilaginous ischemia and resultant permanent laryngeal damage. A traumatic intubation may dislocate these cartilages posteriorly (more often a traumatic curved blade–related complication) or anteriorly (more often a straight blade traumatic complication), which, unless diagnosed early and relocated, may lead to permanent hoarseness.

· The larynx bulges posteriorly into the hypopharynx, leaving deep recesses on either side called the pyriform recesses or sinuses. Foreign bodies (e.g., fish bones) occasionally become lodged there. During active swallowing, the larynx is elevated and moves anteriorly, the epiglottis folds down over the glottis to prevent aspiration, and the bolus of food passes midline into the esophagus. When not actively swallowing (e.g., the unconscious patient), the larynx rests against the posterior hypopharynx such that a nasogastric (NG) tube must traverse the pyriform recess to gain access to the esophagus and stomach. Ordinarily, an NG tube introduced through the right nostril passes to the left at the level of the hypopharynx and enters the esophagus through the left pyriform recess. Similarly, with a left nostril insertion, the NG tube gains access to the esophagus through the right pyriform recess.

· The cricothyroid membrane extends between the upper anterior surface of the cricoid cartilage to the inferior anterior border of the thyroid cartilage. Its height tends to be about the size of the tip of the index finger externally in both male and female adults. Locating the cricoid cartilage and the cricothyroid membrane quickly in an airway emergency is crucial. It is usually easily done in men because of the obvious laryngeal prominence (Adam's apple). Locate the laryngeal prominence, and then note the anterior surface of the thyroid cartilage immediately caudad, usually about one index finger's breadth in height. There is an obvious soft indentation caudad to this anterior surface with a very hard ridge immediately caudad to it. The soft indentation is the cricothyroid membrane, and the ridge is the cricoid cartilage. Because of the lack of a distinct laryngeal prominence in women, locating the membrane can be much more difficult. In women, place your index finger in the sternal notch. Then drag it cephalad in the midline until the first, and ordinarily the biggest, transverse ridge is felt. This is the cricoid ring. Superior to the cricoid cartilage is the cricothyroid membrane, and superior to that, the anterior surface of the thyroid cartilage, then the thyrohyoid space and thyroid cartilage. The cricothyroid membrane is higher in the neck in a woman than a man because the woman's thyroid cartilage is relatively smaller than the man's.

· The cricothyroid membrane measures 6 to 8 mm from top to bottom. If one pierces the membrane in its midportion to perform a retrograde intubation, the puncture point is a mere 3 to 5 mm below the vocal cords, which may not be far enough into the airway to retain the ETT when the wire is cut at the skin. The technique of passing the wire from the outside to the inside of the distal end of the ETT through the Murphy eye enables an additional 4 to 5 mm of insertion, reducing this risk. The proximity of the cricothyroid membrane to the vocal cords is also the driving factor in using small tracheal hooks during surgical cricothyroidotomy to minimize any risk to the cords (see Chapter 15).

Trachea

The trachea begins at the inferior border of the cricoid ring. The sensory supply to the tracheal mucosa is derived from the recurrent laryngeal branch of the vagus nerve. The trachea is between 9 and 15 mm in diameter in the adult and is 12 to 15 cm long. It may be somewhat larger in the elderly. The adult male trachea will generally easily accept an 8.5-mm inner diameter (ID) ETT; a 7.5-mm ID ETT may be preferable in women. If the patient being intubated might require bronchoscopic pulmonary toilette after admission (e.g., chronic obstructive pulmonary disease, airway burns), consider increasing to a 9.0-mm ID tube for men and an 8.0-mm ID tube for women.

Summary

Functional anatomy is important to expert airway management. Attention to the nuances and subtleties of anatomy in relation to technique will often mean the difference between success and failure in managing airways, particularly difficult airways. A clear understanding of the relevant anatomical structures, their blood supply, and their innervation will guide the choice of intubation and anesthesia techniques and will enhance understanding regarding the best approach to each patient. It also provides a basis for understanding how complications are best avoided, or if they occur, how they may be detected.

Evidence

1. General: The reviews by Morris (1) and Redden (2) provide excellent descriptions of the functional anatomy of the upper airway.

2. Nasotracheal intubation: Nasotracheal intubation has largely been supplanted by other methods of emergency airway management that have a higher success rate and fewer complications. Several authors have addressed the complications of nasotracheal intubation (3,4,5,6,7,8,9,10). Some are serious, such as severe epistaxis (1%–10%), intracranial intubation (3), and bronchial obstruction (4). Others are potentially serious, such as retropharyngeal dissection (5,6) and sinusitis, particularly if the nasotracheal tube is left in place longer than 3 to 7 days (7,8). Most immediate complications of nasotracheal intubation are mild and self-limited (e.g., mild to moderate epistaxis) (2,11). Softening the ETT in warm water or saline has been demonstrated to reduce the complication rate, particularly epistaxis (12).

3. Cocaine and coronary vasoconstriction: It is well known that recreational cocaine use is associated with coronary spasm, leading to myocardial ischemia and infarction as well as sudden death (13). It is important to realize that medically administered cocaine to produce nasal vasoconstriction has produced similar complications (14,15,16).

References

1. Morris IR. Functional anatomy of the upper airway. Emerg Med Clin North Am 1988;6:639–669.

2. Redden RJ. Anatomic considerations in anesthesia. In: Hagberg CA, ed. Handbook of difficult airway management. Philadelphia: Churchill Livingstone; 2000:1–13.

3. Marlow TJ, Goltra DD Jr, Schabel SI. Intracranial placement of a nasotracheal tube after facial fracture: a rare complication. J Emerg Med 1997;15:187–191.

4. Skouteris CA, Mylonas AI, Galanaki EJ, et al. Acute bronchial obstruction after nasotracheal intubation: report of a case. J Oral Maxillofac Surg 2002;60:1188–1192.

5. Tintinalli JE, Claffey J. Complications of nasotracheal intubation. Ann Emerg Med 1981;10:142–144.

6. Landess WW. Retropharyngeal dissection: a rare complication of nasotracheal intubation revisited—a case report. AANA J 1994;62:273–277.

7. Holdgaard HO, Pedersen J, Schurizek BA, et al. Complications and late sequelae following nasotracheal intubation. Acta Anaesthesiol Scand 1993;37:475–480.

8. Bach A, Boehrer H, Schmidt H, et al. Nosocomial sinusitis in ventilated patients: nasotracheal versus orotracheal intubation. Anaesthesia 1992;47:335–339.

9. Conetta R, Nierman DM. Pneumocephalus following nasotracheal intubation. Ann Emerg Med 1992;21:100–102.

10. Rhee KJ, Muntz CB, Donald PJ, et al. Does nasotracheal intubation increase complications in patients with skull base fractures? Ann Emerg Med 1993;22:1145–1147.

11. Rosen CL, Wolfe RE, Chew SE, et al. Blind nasotracheal intubation in the presence of facial trauma. J Emerg Med 1997;15:141–145.

12. Lu PP, Liu HP, Shyr MH, et al. Softened endotracheal tube reduces the incidence and severity of epistaxis following nasotracheal intubation. Acta Anaesthesiol Sin 1998;36:193–197.

13. Minor RL Jr, Scott BD, Brown DD, et al. Cocaine induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med 1992;115:797–806.

14. Lange RA, Cigarroa RG, Yancy CW Jr, et al. Cocaine induced coronary artery vasoconstriction. N Engl J Med 1989;321:1557–1562.

15. Ross GS, Bell J. Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epistaxis. Am J Emerg Med 1992;10:219–222.

16. Laffey JG, Neligan P, Ormonde G. Prolonged perioperative myocardial ischemia in a young male: due to topical intranasal cocaine? J Clin Anesth 1999;11:419–424.