Local anesthetic agents (Table 15.1) are weak bases that reversibly inhibit nerve conduction by crossing cell membranes and intracellularly blocking electrically excitable sodium channels. The cationic form of the local anesthetic does not readily cross the cell membrane; thus, tissue acidosis renders local anesthetic agents ineffective, and local anesthetics do not work well if injected into abscesses or areas of cellulitis. Local anesthetics are linear molecules constructed of a hydrocarbon chain separating a lipophilic end from a hydrophilic end. The lipophilic end contains a benzoic acid moiety, and the hydrophilic end contains a tertiary or quaternary amine group. Anesthetics are subdivided based on the type of linkage between the benzoic acid moiety and the hydrocarbon chain. Amide anesthetics (lidocaine, mepivacaine, bupivacaine, etidocaine, prilocaine, and ropivacaine) contain an aminoamide linkage, whereas an aminoester bond characterizes ester anesthetics (cocaine, tetracaine, procaine, chloroprocaine, and benzocaine). The potency of a local anesthetic is related to its lipid solubility. The onset of action is dependent on the relative concentration of un-ionized drug and may be hastened by adding bicarbonate. The duration of action is associated with the degree of protein binding and the local anesthetics peripheral vascular effects. Addition of epinephrine decreases systemic absorption, which increases the duration of the block and decreases the risk of local anesthetic toxicity.

For both classifications of local anesthetics, the type of bond dictates the site of metabolism and route of excretion. Hepatic microsomal enzyme systems degrade the amides into metabolites that possess varying degrees of anesthetic potency. This process can be inhibited in patients with hepatic disease or reduced hepatic blood flow due to congestive heart failure or drugs such as cimetidine or propranolol. Plasma pseudocholinesterase metabolizes the aminoester drugs. This process is more rapid than hepatic metabolism except in patients with a genetically abnormal plasma pseudocholinesterase. The liver produces pseudocholinesterase, so patients with liver dysfunction will also have decreased metabolism of ester local anesthetics.

Lidocaine is both a topical and injectable local anesthetic. A 4% solution is most effective for topical use, whereas 0.5% to 1% solution is effective for injection into soft tissues. To avoid lidocaine toxicity, the recommended safe dosage is 4.5 mg/kg without epinephrine and 7 mg/kg
with epinephrine. Dilutions of 1:100,000 or 1:200,000 of epinephrine are commonly used with injected lidocaine. The lower dose is preferable to minimize the likelihood of side effects and has efficacy equivalent to that of the higher dose. Intravascular absorption of epinephrine may cause hypertension, tachycardia, and arrhythmias. The arrhythmogenic effects of epinephrine can be exaggerated by concurrent use of pancuronium or inhaled anesthetics, particularly halothane. Mepivacaine has an efficacy and toxicity profile similar to that of lidocaine, but mepivacaine has a longer duration of action. The remaining aminoamide local anesthetic agents are less commonly used during otolaryngologic surgery. Bupivacaine, because of its long duration of action, can be used for nerve blocks or infiltrated into wound closures to provide postoperative pain relief. The total dose of bupivacaine injected into the soft tissue of the head and neck should be limited to 2.5 mg/kg when injected alone and 3 mg/kg when mixed with epinephrine.

Cocaine is unique among the topical anesthetics because, in addition to being an excellent topical anesthetic, it is a potent vasoconstrictor. For this reason, cocaine can be used alone in the upper aerodigestive tract for both anesthesia and control of hemorrhage. Cocaine also is unique among local anesthetics in that it is highly addictive and thus one of the most abused drugs. Therefore, cocaine is limited in clinical practice to the mucous membranes of the head and neck. Combinations of lidocaine and epinephrine, phenylephrine, or oxymetazoline have been shown to be as efficacious as cocaine for a number of purposes (1), so many otolaryngologists avoid cocaine. Four percent cocaine has a rapid onset of action (5 to 10 minutes) with duration of action up to 6 hours. Cocaine inhibits the uptake of epinephrine and norepinephrine by adrenergic nerve endings; therefore, it potentiates the effects of catecholamines. The use of cocaine in conjunction with epinephrine risks cardiovascular complications that can prove fatal. The total dose of cocaine applied to the mucosa should be limited to 2 mg/kg. Severe or even fatal toxicity from cocaine can be caused by either central nervous system (CNS) or cardiovascular effects, including coronary artery spasm. Cocaine is metabolized by plasma pseudocholinesterase, and patients with this deficiency are sensitive to the effects of cocaine. Alternatives to cocaine should be highly considered in patients with coronary artery disease, poorly controlled hypertension, a history of arrhythmia, or thyrotoxicosis. Tetracaine is another excellent topical anesthetic agent, especially for ophthalmologic procedures. Although it has 10 times the potency of cocaine, tetracaine lacks the vasoconstrictor effect. Benzocaine, used as a topical spray, produces profound topical anesthesia but can cause methemoglobinemia if used in large doses. This drug is often used as a topical application to the upper aerodigestive tract before endoscopic procedures.

Local anesthetic systemic toxicity (LAST) involves the CNS and cardiovascular system. The signs of CNS toxicity occur early, with tinnitus, circumoral numbness, and agitation serving as early markers and seizures and unconsciousness indicating severe toxicity. The cardiovascular response can range from hypotension to ventricular
dysrhythmias and cardiovascular collapse. Treatment includes immediate management of the airway to prevent hypoxia and acidosis followed by midazolam if a seizure occurs. Advanced cardiac life support (ACLS) protocols should be followed for cardiac arrest, except the only antiarrhythmic considered should be amiodarone. A 20% lipid emulsion bolus (1.5 mL/kg) has proven beneficial, especially to treat bupivacaine, which tightly binds to cardiac sodium channels, resulting in prolonged cardiac arrest. Ropivacaine and levobupivacaine are newer agents, which have efficacy similar to that of bupivacaine but are less cardiac and cerebral toxic (2). Several steps should be taken to reduce the likelihood of LAST, including using the lowest effective dose of local anesthetic and aspirating before each 5-mL injection (3). Unfortunately, an adult patient’s weight or BMI does not correlate with the plasma level after a dose of local anesthetic; thus, the maximum total dose in Table 15.1 should be observed. Acute allergic reactions are uncommon with amide local anesthetics, but may occur with esters, as they are broken down into p-aminobenzoic acid derivatives, a known allergen.

In otolaryngology, local anesthetic techniques are used in procedures such as cosmetic facial surgery, in which distortion of tissue is undesirable. Thus, the goal is to infiltrate small volumes of local anesthetic around the peripheral nerve that supplies the surgical field with sensation. Sensory innervation of the head and neck is primarily from the trigeminal system and the cervical plexus. Effective blockade of sensory branches from these systems necessitates a thorough understanding of the anatomic features of the head and neck (4). This technique involves the use of a 25-gauge needle to infiltrate lidocaine or bupivacaine around sensory nerve branches as they exit the facial skeleton. It is important to avoid direct intravascular injection, as the unintentional injection of a local anesthetic into the vertebral or carotid artery can precipitate a seizure. Therefore, the practitioner should always aspirate before injection of local anesthetic to prevent complications.

Procedures on the face performed with local anesthesia should begin only after the branches of the fifth cranial nerve are blocked. Blocking the supraorbital and supratrochlear nerves with 1 to 3 mL of local anesthetic produces anesthesia of the forehead. The supraorbital nerve is found exiting the orbit in line with the pupil through the supraorbital notch, which can often be palpated. The supratrochlear nerve is approximately 1 cm more medial. Anesthesia of the external nose necessitates blocking the bilateral anterior ethmoidal nerves and infratrochlear nerves. This block is accomplished with either transcutaneous or submucosal injection at the junction of the upper lateral cartilage and the nasal bones laterally that extend superiorly between the medial canthus and the nasal dorsum.

The maxillary branch (V2) of the trigeminal nerve can be blocked in the pterygopalatine fossa with either a transoral approach or a transcutaneous approach, beginning at the coronoid notch and traversing the infratemporal fossa. This block anesthetizes the maxilla, palate, maxillary dentition, and the skin and mucosa of the midface. Procedures that necessitate such extensive anesthesia of the midface are more frequently performed with general anesthesia; therefore, this block is not commonly used. However, blockade of the major terminal branches of the maxillary nerve are common.

Infraorbital nerve block anesthetizes the maxillary incisors, cuspids and bicuspids, associated gingiva, lower eyelid, anterior cheek, and upper lip. Less than 3 mL of solution is necessary. The nerve, which is in line with the pupil and approximately 1 cm below the infraorbital rim, is reached with either an external or sublabial approach. The palate can be anesthetized by blocking the anterior palatine and nasopalatine nerves as they emerge from the greater palatine foramen and incisive canal. Small volumes (0.5 to 1 mL) of anesthetic are needed. During anesthetization of the infraorbital nerve, care must be taken, as injection into bony foramina can cause pressure-induced or needle-induced nerve injury and permanent paresthesia.

The mandibular branch of the trigeminal nerve can be anesthetized at the skull base as it leaves the foramen ovale. The needle is placed through the coronoid notch and across the infratemporal fossa. The injection is made posterior to the lateral pterygoid plate. Blockade of this nerve is used for procedures on the mandible, gingiva, lower teeth, lower lip, anterior two-thirds of the tongue, and floor of the mouth. Most procedures that necessitate this extent of anesthesia are performed with general anesthesia. Peripheral nerve blockade is more commonly applied to branches of the mandibular nerve.

The inferior alveolar nerve can be blocked through a transoral approach as the nerve enters the mandibular foramen in the pterygomandibular space. This technique is commonly used in oral surgery for work on the lower teeth. The injection is immediately medial to the mandibular ramus approximately 1 cm above the occlusal surface of the posterior molars at the anterior-posterior level of the coronoid notch. With this technique, the needle is superior to the medial pterygoid muscle and immediately medial to the mandibular sulcus. Use of this approach commonly blocks the lingual nerve because it is slightly medial and anterior to the inferior alveolar nerve. Anesthesia of the buccal mucosa is accomplished by means of blocking the buccal nerve as it passes over the anterior ramus at the level of the occlusal surface of the molars. Another commonly blocked branch of the cranial nerve V3 is the mental nerve. This blockade is accomplished with an injection at the mental foramen between the two bicuspids at a level immediately below the tooth root apices. The approach can be intraoral or extraoral. In edentulous patients, the location of the foramen can be found in line with the pupil. This technique anesthetizes the lower lip, gingiva, and teeth from the bicuspids to the midline.

Blockade of the cervical plexus anesthetizes the neck, inferior and posterior auricle, and scalp. The cervical plexus arises from the C2, C3, and C4 spinal nerves. These spinal nerves can be blocked as they emerge from the foramina in the cervical vertebrae with an approach lateral to the sternocleidomastoid muscle. This blockade must be performed with care to avoid intrathecal or intravascular injection into the vertebral artery. With injections of large volumes, involvement of the phrenic nerve is likely and thus should be used with caution in patients with respiratory compromise. This technique can be useful in complex surgical procedures on cervical structures, but these procedures usually are performed with general anesthesia. An alternative is to block the cutaneous innervation from the cervical plexus more safely by means of injection of up to 10 mL of local anesthetic at the posterior border of the midpoint of the sternocleidomastoid muscle (Erb point).

Blockade of the superior laryngeal nerve can be attained by means of infiltration of local anesthetic where the nerve enters the thyrohyoid membrane immediately inferior to the lesser cornu of the hyoid bone. This technique blocks sensory innervation from the epiglottis to the vocal cords and facilitates endoscopic procedures and awake fiberoptic intubations.

The characteristics of common inhalational anesthetic agents are given in Table 15.2. These agents exist as liquids at ambient temperature and pressure and are transformed by a vaporizer into gas for rapid absorption and elimination by the pulmonary circulation. After absorption through the alveoli, the agents are distributed to the brain and spinal cord, where the anesthetic effects occur, as well as other tissues throughout the body. The concentration in the brain is directly related to the alveolar concentration. Alveolar and thus brain anesthetic partial pressure are increased by factors that increase anesthetic delivery (higher inhaled anesthetic concentration and alveolar ventilation) and decrease uptake (low solubility and alveolar-venous partial pressure differences). The potency of inhaled anesthetics is defined as the minimum alveolar concentration (MAC). MAC is the concentration that will prevent movement in 50% of patients to surgical incision and is additive between inhalational agents.

The most commonly used volatile inhalational agents are isoflurane, sevoflurane, and desflurane. These halogenated anesthetics are nonflammable and sufficiently potent to be administered as a single anesthetic agent. Halothane was a common agent for many decades, especially in children who needed a mask induction; however, it has been mostly replaced by sevoflurane, which has many advantages, including a smoother mask induction, quicker emergence, less myocardial depression, less arrhythmogenic potential, and a smaller incidence of postoperative liver dysfunction. These halogenated anesthetics have similar effects on cardiac and pulmonary function. In a dosedependent manner over usual clinical doses, these agents increase heart rate and decrease systemic vascular resistance and blood pressure while minimally decreasing cardiac output. Pulmonary effects include a dose-dependent increase in respiratory rate and PaCO2 while decreasing tidal volume and minute ventilation. Increased atelectasis under anesthesia leads to an increased shunt; this usually necessitates an inspired oxygen fraction of at least 25% to 30% to maintain reasonable hemoglobin saturation. Small concentrations of these agents severely depress the ventilatory response to acute hypoxia; therefore, patients must be closely monitored after extubation while being transferred to the post anesthesia care unit (PACU).

Sevoflurane and desflurane are nonflammable, volatile, halogenated agents that are completely fluorinated analogues of isoflurane. Because of low lipid solubility, both agents produce rapid awakening from general anesthesia compared with isoflurane; this difference in emergence time is pronounced in obese patients after prolonged surgery. Because of a high vapor pressure, desflurane requires a special vaporizer to deliver clinically useful concentrations of the gas. Sevoflurane is gentle on the airway and is the preferred agent by most anesthesiologists in pediatric patients that require a mask induction. Although preferred for their quick awakening properties, sevoflurane and desflurane are more costly than isoflurane.

The use of potent inhalational agents for maintenance of anesthesia offers several advantages in head and neck patients. First, the agents decrease bronchoconstriction by relaxing bronchial smooth muscle. Second, they produce reasonable muscle relaxation without the use of neuromuscular blocking drugs, allowing assessment of facial nerve function. Third, inhalational agents produce a moderate degree of hypotension and, in concert with a 15-degree head-up tilt, can reduce surgical blood loss. Hypotension should be used cautiously in elderly patients or patients with a history of hypertension or vascular disease.

Nitrous oxide is an odorless, nonhalogenated inhaled anesthetic often added in concentrations of 50% to 70% (0.5 to 0.7 MAC). Nitrous oxide is highly insoluble, which enables a rapid emergence. It is not a potent inhalational anesthetic, and the brain concentration sufficient to render a patient unconscious may not be achieved at atmospheric pressures. In combination with a halogenated anesthetic, nitrous oxide speeds induction and emergence from general anesthesia, in addition to attenuating some of the cardiovascular and respiratory effects. Although not flammable, nitrous oxide can support combustion, especially if delivered with a high concentration of oxygen, and thus nitrous oxide should not be used during laser endoscopy. Additionally, nitrous oxide quickly diffuses into closed, air-filled body cavities to rapidly expand volume; thus, it must be avoided in the presence of obstructive ileus, pulmonary bullae, or an unrelieved pneumothorax. The middle ear also represents an anatomic air cavity vented to the atmosphere only when the eustachian tube is open. If high concentrations of nitrous oxide are used, the nitrous oxide diffuses into the middle ear faster than nitrogen is able to diffuse out, resulting in an increase in intracavitary pressure that can be great enough to rupture the tympanic membrane or dislodge a graft during otologic surgery. Therefore, common practice is to avoid nitrous oxide or to limit the concentration to 50% and to discontinue administration 30 minutes before graft placement. Nitrous oxide undergoes minimal metabolism by the liver; however, prolonged exposure to high concentrations inhibits methionine synthase activity and can cause megaloblastic or aplastic anemia, although this is not seen with routine intraoperative dosing. Nitrous oxide increases pulmonary artery pressures and should be used cautiously in patients with pulmonary hypertension.

Emergence from a general anesthetic may be more challenging in patients after upper airway procedures. Upon extubation, these patients are more likely to have laryngospasm due to irritation from secretions and blood, which may lead to rapid arterial desaturation. If the anesthesiologist is unable to give positive-pressure ventilation by mask, jaw thrust should be exerted with pressure between the mandible and the mastoid process. If laryngospasm persists, an intravenous anesthetic should be administered and then a small dose of succinylcholine (20 mg) if necessary.

All of the inhaled halogenated anesthetics are triggers for malignant hyperthermia, a rare but well-known reaction. Malignant hyperthermia occurs more commonly if succinylcholine has been used for muscle relaxation. Characteristics of malignant hyperthermia include tachycardia, markedly increasing PaCO2, metabolic acidosis, sustained muscle rigidity, myoglobinuria, and an increasing temperature (may be a late sign). These are manifestations of a generalized hypermetabolic state initiated by an inhibition of calcium reuptake into the sarcoplasmic reticulum of the skeletal muscle. If not controlled swiftly, malignant hyperthermia is fatal. The principles of management include discontinuing all volatile anesthetics and succinylcholine, hyperventilating with 100% oxygen, administering dantrolene 2.5 mg/kg up to 10 mg/kg, administering bicarbonate as needed to correct the metabolic acidosis, and total-body cooling. The surgery should be stopped as soon as possible. Any patient with a history
or family history of malignant hyperthermia should not receive halogenated anesthetic agents or succinylcholine for future procedures.

For most surgical procedures, the first step in production of general anesthesia is intravenous administration of a hypnotic drug, followed by maintenance of anesthesia with an inhalational agent supplemented with narcotics. The intravenous induction is usually more acceptable to the patient than inhalation induction with a volatile agent. The drugs commonly used for this purpose share the ability to produce a state of unconsciousness rapidly, which coincides with a critical peak concentration in brain tissue. Awakening occurs when this concentration decreases, usually through redistribution of the drug from brain tissue to muscle and adipose tissue. Metabolism and excretion of the drug then take place in the liver and other organs (Table 15.3), but this is only of consequence for doses larger than for induction, such as in prolonged infusions.