ANESTHESIA FOR NOSE AND THROAT SURGERY

Functional Anatomy of the Larynx

The larynx allows respiration and speech,^{[93] [94]} and laryngeal reflexes protect the airway. Swallowing activates the glottic closure reflex to prevent aspiration. Many other sensory stimuli that affect the superior laryngeal nerve will also activate this basic primitive reflex. The false vocal cords are ventricular folds that act as a muscular valve that closes because of pressure from below to stop air going out. The true vocal cords act like a one-way entrance valve that resists pressure from above but not from below.^[93] When the true vocal cords are in spasm, sudden positive pressure from above may not be enough to move air into the lungs.

The vagus nerve provides the nerve supply to the larynx. Sensory innervation of the larynx down to the vocal cords is supplied by the superior laryngeal nerve. The superior laryngeal nerve comes from the inferior ganglion of the vagus. The internal branch of the superior laryngeal nerve consists mostly of sensory fibers, with a few motor fibers leading to the arytenoid muscles. The internal branch divides into upper and lower branches. The upper branch provides sensory innervation to the mucosa of the lower part of the pharynx, the epiglottis, the vallecula, the arytenoepiglottic folds, and the laryngeal vestibule. The lower branch passes close under the surface of the mucosa of the piriform fossa and supplies sensory innervation to the arytenoepiglottic folds and posterior rima glottidis. The recurrent laryngeal nerves provide sensory innervation below the true vocal cords and into the upper part of the trachea. Sensory innervation is denser at the glottic inlet. The lower half of the true vocal cords has more touch receptors. The epiglottic and supraglottic areas have chemical and thermal receptors.^[93]

The recurrent laryngeal nerves provide motor innervation to all the intrinsic laryngeal muscles, except the cricothyroid and inferior pharyngeal constrictors. These muscles receive motor innervation from the external branch of the superior laryngeal nerve ( Fig. 65-1 ).

The intrinsic laryngeal muscles consist of the following:

1. The posterior cricoarytenoids abduct the vocal cords and widen the glottic chink during respiration.
2. The thyroarytenoids and lateral cricoarytenoids adduct the vocal fold (false cords).
3. The interarytenoids close the posterior gap in the glottis (posterior commissure) by abduction.
4. The cricothyroids adduct and tense the true vocal cords.
5. The vocalis muscle also shortens the true vocal cords.
6. The arytenoepiglottics and oblique arytenoids narrow the glottic inlet by adduction of the arytenoepiglottic folds.

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Figure 65-1 Intrinsic laryngeal muscles and their innervation. (From Schuller DE, Schleuning AJ: Otolaryngology—Head and Neck Surgery, 8th ed. Mosby-Year Book, 1994, p 252.)

Endotracheal intubation, neck surgery, or stretching of the neck can injure the recurrent laryngeal nerve. The resulting position of the vocal cords depends on whether the injury is unilateral or bilateral and whether the external branch of the superior laryngeal nerve is involved.

Unilateral recurrent laryngeal nerve injury causes the cord on the injured side to assume a paramedian position because the unopposed action of the ipsilateral cricothyroid muscle adducts the cord toward the injured side. If the external branch of the superior laryngeal nerve is also involved, the true vocal cord will be more medial and less tense. The voice is weak and hoarse, and the risk of aspiration increases. Eventually, the muscles compensate somewhat, and the cord becomes more medially positioned.

In bilateral vocal cord paralysis, both cords usually lie within 2 to 3 mm of the midline in the adducted position. Although the voice is of limited strength, it is generally of good quality. The airway is often inadequate. Stridor and dyspnea can occur with even modest exertion. Life-threatening airway obstruction occurs when the cords become infected or edematous. Bilateral recurrent laryngeal nerve injury that results in unopposed cricothyroid muscle contraction is one mechanism of bilateral vocal cord paralysis. Vocal cord paralysis may also result from lesions at the nucleus ambiguus, its supranuclear tracts, and the main trunk of the vagus nerve itself. The anatomy of the recurrent laryngeal nerves makes them potentially vulnerable to injury during surgery. They course around the subclavian artery on the right and the aorta on the left. They are especially likely to be injured during thyroid and cervical spine surgery. Such patients may require a tracheostomy.^[95]

Laryngospasm

Laryngospasm is a reflex closure of the upper airway from spasm of the glottic musculature. This form of airway obstruction is common in children. It is associated with light planes of anesthesia and the presence of foreign matter irritating the vocal cords. Laryngospasm is mediated by the superior laryngeal nerve. This strong glottic closure reflex can persist even after irritation of the mucosa ceases.^[96] During a laryngospasm, the false cords and epiglottic body come together firmly. There may be no airflow or vocal sound, and the true vocal cords cannot be seen. The extrinsic muscles of the larynx (especially the thyroid) may also be involved and help create a muscular ball-valve mechanism. In addition, stimulation of the superior laryngeal nerve can cause a reflex apnea by inhibiting medullary inspiratory motor neurons and decreasing phrenic nerve activity.

The intravenous administration of lidocaine, topical application of cocaine, and deep levels of anesthesia attenuate the effect of the stimulus and the activity of the superior laryngeal nerve and thereby decrease the likelihood of prolonged glottic closure. Intravenous fentanyl

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Although laryngospasm can often be disrupted by applying sustained positive pressure and increasing the depth of anesthesia with intravenous propofol or other intravenous drugs, sometimes muscle relaxation (e.g., with succinylcholine, 10 to 50 mg IV) is needed to allow the patient to be ventilated. Failure to treat laryngospasm in a timely manner is dangerous. In addition to hypoxemia, some patients who are able to generate very large negative inspiratory pressures when attempting to breathe against the obstruction may succumb to "negative-pressure pulmonary edema." ^[97] The anesthesiologist needs to take a proactive approach to preventing and terminating laryngospasm.

Stridor

Stridor is noisy inspiration from turbulent upper airway gas flow. It is frequently seen with airway obstruction and always commands attention. Wherever possible, attempts should be made immediately to establish the cause of the obstruction. Endoscopy can be particularly useful.

The first issue of clinical concern in the setting of stridor is whether intubation is immediately necessary. If intubation can be delayed for a period, a number of potential options can be considered:

• Expectant management with oxygen by facemask and positioning the head up at 45 to 90 degrees

• Nebulized racemic epinephrine

• Dexamethasone (Decadron), 4 to 8 mg intravenously every 8 to 12 hours, in patients with airway edema

• Heliox (e.g., 70% helium, 30% oxygen)

Heliox has been used for decades for the treatment of acute airway obstruction.^[98] The usual respiratory airflow is laminar, and resistance is dependent on gas viscosity. In the setting of airway obstruction, however, airflow becomes turbulent and dependent on gas density. Because heliox has a density roughly a third that of air or oxygen, it can lead to a dramatic decrease in airway resistance and improvement in ventilation.^{[99] [100] [101]}