Anesthesia for Head and Neck Surgery



Superlative surgical outcomes rarely occur by chance but are the product of a complex process that starts long before the day of surgery and lasts for at least 30 days after. This process is based on two factors: (1) active perioperative optimization of the patient’s medical comorbidities and (2) consistent surgical and anesthetic approaches to procedures. To achieve this goal, active collaboration and communication with anesthesiologists, internists, and other consultants is necessary throughout the perioperative period. Anesthesiologists are uniquely situated in the health care system to implement the “perioperative surgical home” model of care. Therefore, anesthesia for head and neck surgery includes an understanding of pharmacology, fluid, airway, and medial comorbidity management to act as a framework for these collaborations.

Anesthetic agents are classified by their primary actions; sedative hypnotics, amnestic, analgesics, and muscle relaxants. Most agents provide a combination of these effects and can be utilized solely or in combination with one another to provide surgical conditions and minimize patient risk.

Continuum of Depth of Sedation


  • Minimal sedation anxiolysis

    1. Normal response to verbal stimuli

  • Moderate sedation/analgesia (“conscious sedation”)

    1. Active response to verbal or tactile stimuli

  • Deep sedation/analgesia

    1. Active response to painful stimuli only

  • General anesthesia

    1. Unarousable to any stimuli

It is critical to understand that only the patient’s response to stimuli defines the level of sedation. Therefore, the level of sedation is never defined by a particular anesthetic agent, its dose, or the airway management technique or device utilized. For example, it is possible, in a very rare patient, to achieve the level of general anesthesia with propofol and a nasal cannula or conversely an intubated patient with minimal sedation anxiolysis. Additionally, any level of sedation may be combined with local anesthetics, nerve blocks, or nonsedating systemic analgesics to improve surgical conditions and decrease patient risk. Monitored anesthesia care is not synonymous with moderate sedation or any particular pharmacological agents. MAC is defined by the anesthesiologist’s ability to assess the patient, anticipate physiological derangements, and medical sequelae of the procedure as well as the anesthesiologist’s ability to intervene to rescue a patient’s airway and convert to general anesthesia if required.

A majority of patients have some degree of apprehension concerning an upcoming surgical procedure, and more often than not, the “anesthesia” figures prominently in this anxiety. It is therefore crucial that the anesthesiologist devotes the necessary time to explain the sequence of events comprising the anesthetic and to thoroughly answer any questions that patients or their family may have.

Anesthetic Agents

Sedative Hypnotics and Amnestics

In general, it is thought that anesthetics act by reversibly inhibiting neurosynaptic function of various regions or components of the cell membrane, either through action on membrane proteins or lipids or through modulation of the inhibitory neurotransmitter gamma-amino butyric acid (GABA). Because these compounds are involved in a number of multisynaptic pathways, they have repercussions far beyond their local sites of action. By altering sympathetic tone, these agents affect almost all organ systems, especially the cardiovascular system.

Each of these drugs has advantages and disadvantages in its clinical profile, so that no one drug can be considered the “ideal” agent in all circumstances.

Combinations of various drugs, such as benzodiazepines and opioids along with propofol, ketamine, and etomidate, can be titrated to the desired level of consciousness. These, in turn, can also be combined with volatile anesthetics and gases. The permutations of these mixtures are endless and can be thoughtfully tailored to the comorbidities of the patient and the surgical necessities.

Intravenous Anesthetics Thiopental’s

(Ultra-short-acting barbiturate) widespread use has come to a close and is not available in the United States currently, but it is encountered in other countries. It is associated with cardiac and respiratory depression and may accumulate after repeated doses, thereby prolonging emergence. It is a highly effective treatment of last resort for status epilepticus. The usual induction dose is 3 to 5 mg/kg IV. Once popular in the United States, secobarbital and pentobarbital are now only encountered when on foreign medical missions. Methohexital is the last remaining available agent in this class. It can be used for procedural sedation but is generally reserved for electroconvulsive therapy due to its unusual ability to lower the seizure threshold.

Propofol’s proposed mechanism of action is as a potentiator of the GABAA receptor. It is an IV sedative hypnotic agent that rapidly produces hypnosis, usually within about 40 seconds, and is quickly eliminated with minimal accumulation after repeated doses, allowing for a rapid return to consciousness. Propofol has also been associated with a lesser incidence of nausea and vomiting. Therefore, it is the most common agent of choice for induction of general anesthesia (1.5-2.5 mg/kg) and for deep procedural sedation (given as boluses of 10-20 mg or as an infusion of 25-75 µg/kg/min). Its advantages make it particularly suited to outpatient surgery. It is also associated with several important side effects: arterial hypotension (about 20%-30% decrease), apnea, airway obstruction, and subsequent oxygen desaturation. The therapeutic window between sedation, deep sedation, and general anesthesia is very narrow. These facts have earned it a Food and Drug Administration (FDA) black box warning, stating that “the agent should be administered only by those trained in the administration of general anesthesia and not involved in the procedure.”

Etomidate, a GABAA receptor modulator, rapidly induces general anesthesia while preserving ventilatory drive, cardiovascular stability, and decreasing intracranial pressure. However, etomidate also causes suppression of corticosteroid synthesis and can lead to primary adrenal suppression. As always, all of its effects must be considered with patient selection.

Ketamine, a phencyclidine derivative that acts as an NMDA (N-Methyl-D-Aspartate) receptor antagonist, induces dissociative anesthesia in which patients are unresponsive to noxious stimuli but may appear to be awake. Pharyngeal and laryngeal reflexes and respiratory drive also remain intact until very deep levels of anesthesia are attained. Additionally, ketamine has potent analgesic properties (through action on the NMDA receptor) and is, therefore, useful as a low-dose infusion (0.1-0.2 mg/kg/h) for repeated dressing changes, opiate-sparing postoperative analgesic, or as an opiate-sparing adjunct to general anesthesia. Ketamine produces increased intracranial pressure (ICP), tachycardia, and a dysphoric reaction, all of which should be considered in patient selection and subsequent monitoring. Of note, recent data suggest that prolonged low-dose infusions (8-72 hours) are therapeutic in the treatment of depression and chronic pain syndromes. Additionally, ketamine is an effective bronchodilator.

Dexmedetomidine, an alpha-2 adrenergic agonist, is a relatively new sedative hypnotic with minimal analgesic properties. It maintains ventilatory drive and is, therefore, useful during airway examinations or intubations. However, this medication is usually administered as a continuous infusion (0.2-1 µg/kg/h) that is preceded by a 10-minute loading dose (1 µg/kg/10 min). This is due to its ability to cause hypotension, bradycardia, and even asystole when titrated too rapidly.

Benzodiazepines have enjoyed widespread popularity because of their ability to reliably provide amnesia, reduce anxiety, and increase the seizure threshold without undue respiratory or cardiovascular depression. The three most commonly used benzodiazepines are diazepam (Valium), lorazepam (Ativan), and midazolam (Versed). Midazolam has several advantages: it is water soluble, which reduces the pain of injection associated with diazepam; it is approximately twice as potent as diazepam, with a more rapid peak onset (30-60 minutes) and an elimination half-time of 1 to 4 hours. It is, therefore, well suited to shorter procedures where extubation is anticipated or for sedation during local anesthesia (1-2 mg IV in adults). Recent papers have suggested that use of midazolam produces a higher rate of postoperative delirium in the elderly and other at-risk populations (posttraumatic stress disorder patients).

The specific benzodiazepine antagonist is flumazenil (Romazicon), which is supplied in solutions containing 0.1 mg/mL. The recommended dose is 0.2 mg IV over 15 seconds, which can be repeated every 60 seconds for four doses (1 mg total) with more than 3 mg over 1 hour is advised. It is important to note that flumazenil’s half-life (t1/2) is 7 to 15 minutes and that repeated dose may be required over an extended period when it is used to treat overdosing of long-acting benzodiazepines (lorazepam’s t1/2 is 9-16 hours).

Droperidol, a butyrophenone, has been used extensively in the past as a sedating agent. However, in 2001 the FDA included a black box warning for this medication, citing data of QT prolongation and torsade de pointes when given at higher doses of 2.5 to 7.5 mg. Subsequently, 0.625 to 1.25 mg of droperidol is occasionally used for its antiemetic properties. This is done with active ECG monitoring only and is contraindicated in patients with QT intervals that are lengthy at baseline.

Haloperidol (Haldol), a butyrophenone, is a long-acting antipsychotic medication that may be useful in treating acute delirium in the postoperative period. However, due to the QT prolongation that it produces its routine use is not recommended.

Diphenhydramine (Benadryl), an antihistamine, has sedative and anticholinergic as well as antiemetic properties. The usual dose is 25 to 50 mg pod, IM, or IV. Because it blocks histamine release, it can be used in conjunction with steroids and H2 blockers as prophylaxis for potential allergic reactions.

Inhalation Agents

The inhalation anesthetics are those volatile agents and gases that are administered via the lungs. They are administered by mask or through an endotracheal tube, attain a certain concentration in the alveoli, diffuse across the alveolar-capillary membrane, and are transported by the blood to their sites of action in the central nervous system (CNS). Many factors affect the uptake and distribution of the volatile agents, including agent concentration, minute ventilation, diffusion capacity across the alveolar membrane, blood-gas partition coefficient (solubility), cardiac output, alveolar-arterial gradient, and the blood-brain partition coefficient.

The potency of the inhalation anesthetics is usually described in terms of minimal alveolar concentration (MAC). This is defined as the concentration of anesthetic at one atmosphere that will prevent movement in response to a surgical stimulus (surgical incision) in 50% of individuals. This allows for a somewhat quantitative assessment of the amount of anesthetic delivered. MAC decreases by 6% per decade of age increase, producing a 25% decrease in MAC for a 70-year-old patient versus a 30-year-old patient. It should be noted that MAC is additive; for example, if one-half MAC of two agents is delivered simultaneously, this is equivalent to one MAC of a single agent. Therefore, fractions of MAC of several anesthetic agents, inhalational and intravenous, can be combined to provide adequate anesthesia with reduced side effects from large doses of any one agent.

Nitrous Oxide (N2O)

  • MAC: 104% (therefore, one MAC of N2O cannot be delivered)

  • Blood-gas partition coefficient: 0.47

N2O is a sedative hypnotic that has profound analgesic properties, but importantly no amnestic effects. It is mainly used as a short-term adjunct to general anesthesia at 30% to 70%. This is due to four properties: (1) rapid onset and offset, (2) potentiation of volatile anesthetics via the second gas effect, (3) improved cardiac stability, and (4) analgesia. These advantages are offset by N2O role in postoperative nausea and vomiting (PONV) and its expansion of air-filled spaces. Because N2O is 34 times more soluble than nitrogen, N2O can double the volume of a compliant air-filled space in 10 minutes and triple it in 30 minutes. Of clinical importance, N2O may cause a significant expansion of the closed middle ear space and potential disruption of a tympanic graft. For this reason, N2O is not used during procedures involving air-filled closed spaces or when a patient is at risk of a pneumothorax. Additionally, air-filled cuffs are also subject to this effect and cuff pressure should be carefully monitored when nitrous oxide is in use.


  • Type: Halogenated methyl ethyl ether

  • MAC:1.15%

  • Blood-gas partition coefficient: 1.4

  • Uses: Isoflurane is rarely used in modern anesthetic practice, but found in developing nations. It is the most soluble of the volatile agents, therefore it is eliminated most slowly and produces the prolonged emergence.

  • Notes: Recently isoflurane has been linked to a possible increase in postoperative cognitive dysfunction in the elderly and increased risk of neurodegeneration in pediatric patients. The FDA and the anesthetic community are actively investigating these concerning issues.


  • Type: Fluorinated methyl isopropyl ether

  • MAC: 2.2%

  • Blood-gas partition coefficient: 0.6

  • Uses: Suitable for inhalational inductions

  • Notes: When used with heated desiccated and exhausted soda lime, it has been shown to produce the nephrotoxin compound A. Frequent changes to fresh soda lime and fresh gas flows above 2 L/min have eliminated this risk. It also decreases airway irritability and can be used to treat status asthmaticus.


  • Type: Fluorinated methyl ethyl ether

  • MAC: 6%

  • Blood-gas partition coefficient: 0.42

  • Uses: It is the least soluble of the volatile agents, therefore it is eliminated most rapidly. This produces a shortened emergence and is suitable for use in obese patients, as it does not readily accumulate in adipose tissue.

  • Notes: Requires a heated vaporizer because of its lower partial pressure.

  • At concentrations above 10%, desflurane produces clinically significant tachycardia and airway irritability. This combined with its pungent odor make it unsuitable for inhalation inductions.

Muscle Relaxants

All volatile anesthetics and sedative hypnotics will provide varying degrees of muscle relaxation when given at the appropriate dose. There are, however, surgical procedures when patient movement is extremely detrimental to their outcome and these procedures warrant the use of other agents to ensure muscle relaxation.

Neuromuscular Blocking Drugs

Neuromuscular blocking drugs are capable of interrupting nerve impulse conduction at the neuromuscular junction. This allows for muscle relaxation, which is used to facilitate intubation of the trachea and to provide for optimum surgical working conditions. They can be classified as either depolarizing muscle relaxants, of which succinylcholine is the only clinically available example, or nondepolarizing muscle relaxants. There are many nondepolarizing muscle relaxants, but currently only vecuronium, atracurium, rocuronium, and cisatracurium are readily available. Pancuronium and mivacurium are unavailable in the United States due to marketing and manufacturing issues.

The nondepolarizing agents can be further subdivided into short-, intermediate-, and long-acting drugs.

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Succinylcholine Onset: 30-60 sec Duration: 5-10 min
Rocuronium Onset: 60-90 sec Duration: 45-70 min
Vecuronium Onset: 90-180 sec Duration: 30-40 min
Atracurium Onset: 60-120 sec Duration: > 30 min
Cisatracurium Onset: 90-120 sec Duration: 60-80 min

Monitoring of neuromuscular blockade is accomplished by a supramaximal electric stimulation delivered to a muscle via a neuromuscular stimulator. Decreased twitch height (depolarizing relaxants) or fade (nondepolarizing relaxants) to either train-of-four (four 2-Hz impulses in 2 seconds) or tetanus (50-100 Hz for 5 seconds) is proportional to the percentage of neuromuscular blockade. In this way, with at least one twitch of a train-of-four present, reversal of the blockade can be reliably achieved. Reversal is primarily accomplished with neostigmine 40 to 75 µg/kg and as second choices edrophonium 1 mg/kg or pyridostigmine 0.2 mg/kg. These acetylcholinesterase inhibitors cause accumulation of acetylcholine at the neuromuscular junction, thereby facilitating impulse transmission and reversal of the blockade. Of importance, anticholinergic drugs (glycopyrrolate or atropine) must accompany administration of the reversal agents to avoid the undesirable muscarinic effects (only the nicotinic, cholinergic effects are necessary). Occasionally, prolonged neuromuscular blockade is required postoperatively. In these cases, it is of the utmost importance to monitor the patient’s depth of sedation using a spectral index (BIS) monitor, which is a form of electroencephalograph (EEG), while the patient is rendered incapable of voluntary and involuntary movement.

Sugammadex, the first selective relaxant-binding agent, encapsulates and rapidly reverses the effects of rocuronium and vecuronium. Since its approval by the FDA in 2015, sugammadex (Birdion) has been widely incorporated into clinical practice especially for surgical procedures where nerve monitoring is required. Optimal intubation conditions can be achieved with rocuronium and then reversed with sugammadex. This technique has eclipsed the use of succinylcholine, thereby avoiding the muscle aches and risk of hyperkalemia associated with succinylcholine. Two major caveats must be noted with the use of squamae (1) it is not recommended in patients with renal impairment and (2) it may bind progesterone and reduce the effectiveness of oral contraceptives. Therefore, these patients must be informed to use an additional alternate method of contraception for the 7 days following exposure.


Before pain is treated, it is of the utmost importance to diagnose its character, acute or chronic, and its etiology. Only then can the correct therapeutic modality be selected. It is dangerous to ever assume the cause of a patient’s pain before examining or conferring with them. Neglecting these steps is to risk missing critical clinical events and to put your patient in harm’s way.

Local Anesthesia


Local anesthesia is the blockade of sensation in a circumscribed area. Local anesthetics interfere with the functioning of the sodium channels, thereby decreasing the sodium current. When a critical number of channels are blocked, propagation of a nerve impulse (action potential) is prevented, as in the refractory period following depolarization. All of the clinically useful agents belong to either the aminoester or aminoamide groups. In addition, they are all diffusible, reversible, predictable, water soluble, and clinically stable and they do not produce local tissue irritation.


Local anesthetics consist of three parts: tertiary amine, intermediate bond, and an aromatic group. The intermediate bond can be either of two types: ester (R-COO-R) or amide (R-NHCO-R); local anesthetics are therefore classified as aminoesters or aminoamides.

In general, there are three basic properties that will influence their activity:

  1. Lipid solubility: This will affect the potency and duration of effect.

  2. Degree of ionization: According to the Henderson-Hasselbalch equation, the local hydrogen ion concentration will determine where chemical equilibrium lies. The greater the pKa, the smaller the proportion of nonionized form at any pH. The ester pKa values are higher than the amide, accounting for their poor penetrance. The nonionized form is essential for passage through the lipoprotein diffusion barrier to the site of action. Therefore, decreasing the ionization by alkalinization will increase the initial concentration gradient of diffusible drug, thereby increasing the drug transfer across the membrane. Importantly, infected tissues have a decreased pH and causes less nonionized drug to be present (or more ionized drug), and therefore a lesser concentration of drug at the site of action, resulting in a poor or nonexistent local block. Blocking the relevant nerves proximally to the CNS in healthy uninfected tissue can circumvent this effect.

  3. Protein binding: A higher degree is seen with the longer-acting local anesthetics.

Uptake, Metabolism, and Excretion

Most local anesthetic agents diffuse away from the site of action in the mucous membranes and subcutaneous tissues and are rapidly absorbed into the bloodstream. Factors that affect this process are the physicochemical and vasoactive properties of the agent: the site of injection, dosage, presence of additives such as vasoconstrictors in the injected solution, factors related to the nerve block, and pathophysiologic features of the patient. Certain sites of particular interest to the otolaryngologist (eg, laryngeal and tracheal mucous membranes) are associated with such a rapid uptake of local anesthetics that the blood levels approach those achieved with an intravenous injection.

Amide local anesthetics are metabolized by the liver in a complex series of steps beginning with N-dealkylation. Ester drugs are hydrolyzed by cholinesterases in the liver and plasma. Both degradation processes depend on enzymes synthesized in the liver; therefore, both processes are compromised in a patient with parenchymal liver disease. Many of the end products of catabolism of both esters and amides are excreted to a large extent by the kidneys. Catabolic by-products may retain some activity of the parent compound and may, therefore, contribute to toxicity.


A toxic blood level of local anesthetic can be achieved by rapid absorption, excessive dose, or inadvertent intravascular injection.

Significant symptoms of local anesthetic systemic toxicity are predominantly confined to the CNS and cardiovascular system. The CNS responses to local anesthetic toxicity begin with an excitatory phase, followed by depression. The extents of these symptoms are dose dependent and include circumoral paresthesias, tinnitus, and mental status changes. They can progress to tonic-clonic seizures and eventual coma, producing respiratory depression and respiratory arrest. Initial symptoms can be treated with benzodiazepines such as diazepam or less effectively midazolam, always remembering that they too can exacerbate respiratory depression. Should seizures ensue, symptomatic therapy should continue with the above-mentioned drugs and an adequate airway and oxygenation must be ensured.

Local anesthetics exert direct dose-related depressive effects on the cardiovascular system. Increasing levels of local anesthetics diminishes both myocardial contractility and peripheral vascular tone. Toxic doses of local anesthetics can produce rapid and profound cardiovascular collapse. If local anesthetic systemic toxicity occurs, ACLS (advanced cardiac life support) protocols should be instituted immediately. During ACLS an initial dose of 1.5 mL/kg, 20% lipid emulsion (Intralipid) should be administered. If needed, this dose can be followed by additional doses and an infusion of 0.5 mL/kg/min, up to a 30-minute maximal dose of 10 mL/kg. In cases where this protocol has been followed, a full recovery of the patient has resulted. Intralipid therapy may also be instituted to treat CNS local anesthetic toxicity. Please refer to for additional information.

Epinephrine is often added to local anesthetic mixtures to increase the duration of the nerve block, to decrease systemic absorption of the local anesthetic, and to decrease operative blood loss. In commercially prepared solutions of local anesthetics, epinephrine is usually found in a 1:100,000 (1 mg/100 mL) or 1:200,000 (1 mg/200 mL) concentration. Tachycardia and hypertension are the most common side effects of this medication and can be treated with short-acting beta-adrenergic blocking drugs (esmolol). Hypertensive crisis can be precipitated by epinephrine in patients taking tricyclic antidepressants and monoamine oxidase inhibitors. Epinephrine toxicity can produce restlessness, nervousness, a sense of impending doom, headache, palpitations, and respiratory distress. These symptoms may progress to ventricular irritability and seizures.

True allergic reactions to local anesthetics account for less than 1% of all adverse reactions and most commonly are attributed to the methylparaben or metabisulfite preservative. True allergy to local anesthetics is more common among ester derivatives; it is extremely rare among the amide local anesthetics.

Choosing the anesthetic technique for a patient with a history of local anesthetic allergy is a not infrequent clinical problem. A careful history with documentation, if possible, should help sort out those with toxic reactions from those with true allergy. Some authorities have advocated provocative intradermal testing, but this should only be undertaken when prepared to treat anaphylaxis and can still be unreliable. Alternatively, some authors suggest using a preservative free local anesthetic from the opposite class of the one suspected. If doubt still exists, one must consider alternative techniques, such as general anesthesia.

Both prilocaine and benzocaine can reduce hemoglobin to methemoglobin, which has a diminished ability to transport oxygen to the peripheral tissues. (Note: A pulse oximeter cannot measure methemoglobin. If significant quantities of methemoglobin are present, the oxygen saturation will read 85% regardless of what the actual saturation is and, therefore, may be grossly in error and unreliable.) Patients with glucose-6-phosphate deficiencies are more susceptible to methemoglobinemia. The treatment of methemoglobinemia is intravenous administration of a 1% methylene blue solution to a total dose of 1 to 2 mg/kg.

Local Anesthetic Agents

Aminoester Agents

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Apr 30, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on Anesthesia for Head and Neck Surgery
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