Manual of Emergency Airway Management, 3rd Edition

8.Sedation and Anesthesia for Awake Intubation

Michael F. Murphy

Description

Humans protect their airway at virtually any cost. In fact, it is generally impossible to get even a glimpse of the glottis with a laryngoscope in a fully awake and aware patient. This is why the “awake” methods of laryngoscopy referred to in the difficult airway algorithm always enclose the term awake in quotation marks, meaning that although the patient may be nominally aware, his or her sensibilities are attenuated by local anesthesia, sedation, or both.

Ordinarily, local anesthesia and sedation are used concurrently for diagnostic or therapeutic upper airway interventions in patients. If the patient is uncooperative or when time is of the essence, systemic sedation dominates and less local anesthesia is used. Cooperative patients requiring nonemergent diagnostic maneuvers tend to receive more local anesthesia and less systemic sedation because there is sufficient time to dry the airway of secretions and perform the various local anesthesia techniques.

Awake laryngoscopy has two main roles, both of which apply to patients with anticipated difficult intubation: (a) to determine whether intubation will be feasible, thus facilitating a decision regarding the use of neuromuscular blocking agents, and (b) to intubate, particularly in circumstances in which the patient's airway may be deteriorating, as in angioedema or upper airway burns or trauma (“the dynamic airway”). An awake look intended to determine the feasibility of intubating the trachea nasally or orally can be accomplished in two ways. First, a flexible fiberoptic bronchoscope or nasopharyngoscope inserted through the nostril may be used to determine if nasal intubation is feasible or to locate the glottis in patients suffering from blunt or penetrating neck trauma to determine if orotracheal intubation will be possible. Topical nasal anesthesia and minimal, if any, sedation are usually all that is required. Second, a standard or video laryngoscope blade is inserted into the mouth as for a direct laryngoscopy, with the intention of confirming that glottic visualization (and, thus, orotracheal intubation) is possible.

Substantial local anesthesia of the mouth, oropharynx, and hypopharynx, or very deep sedation, is usually required to obtain an adequate view of the glottis using this technique. If the glottis is adequately visualized, then the airway manager may elect to proceed immediately to an awake intubation or withdraw the laryngoscope and perform rapid sequence intubation (RSI). The approach will be dictated by the clinical circumstance. In general,

· If the difficult airway is dynamic (i.e., evolving) and is the reason for the intubation, then it is usually advisable to intubate the patient during the awake direct laryngoscopy, if possible, because the airway may deteriorate significantly over time or as a result of the direct laryngoscopy. A good rule of thumb is, if the airway might change, intubate it when you have the chance.

· If the difficult airway is chronic (e.g., cervical rheumatoid arthritis) and is not the reason for the airway crisis but simply a confounder to the intubation, then it is reasonable to withdraw the laryngoscope and perform a proper RSI, in the knowledge that the airway is not going to deteriorate further while the RSI is being done.

An awake intubation is more invasive and requires greater degrees of local anesthesia, sedation, or, usually, both.

Indications and Contraindications

Awake intubation is indicated when the individual responsible for airway management is not confident that gas exchange will be assured by any or all of these techniques if the patient is rendered apneic: bag-mask ventilation (BMV), extraglottic device (EGD), or intubation. This is particularly important if an awake laryngoscopy has confirmed that intubation will be challenging. Sedation, upper airway local anesthesia, or both may be indicated for the insertion of nasal and oral airways or an extraglottic rescue device, such as a laryngeal mask airway or Combitube.

Similarly, sedation or local anesthesia of the upper airway may be indicated to facilitate upper airway evaluation (e.g., endoscopy) to identify the location of foreign bodies and remove them, identify a cause of hoarseness, evaluate airway integrity in blunt and penetrating neck trauma, diagnose epiglottitis in a patient with throat pain out of keeping with the oropharyngeal examination, and others.

There are really no contraindications to the use of local anesthetic agents and systemic sedation to enable upper airway evaluation, particularly in an emergency. However, there are some precautions with respect to the choice of sedative agents and how they are used.

Sedation Techniques

An awake look in an emergency airway situation relies almost entirely on the intravenous (IV) titration of systemically active sedation. There is usually not enough time to produce adequate local anesthesia of the oropharynx and the hypopharynx for a patient to tolerate an awake look procedure without at least a moderate level of sedation. The level of sedation sought is similar to that used for painful procedures in the emergency department, such as reduction of a dislocated shoulder or drainage of a deep cutaneous abscess.

A variety of sedating-type medications may be used, including midazolam, propofol, etomidate, ketamine, and others. In the emergent situation, when judicious chemical restraint is required to permit airway examination of combative and intoxicated patients, haloperidol, a butyrophenone, can be immensely helpful. IV doses of 2 to 10 mg in the adult can be carefully titrated to effect at 3 to 5 minute intervals.

Two medications have been employed in anesthetic practice that may show promise for use in the emergency department awake look situation: remifentanil and dexmedetomidine. Remifentanil is an ultrashort-acting medication that, given by bolus injection or by infusion, has a rapid onset and offset, both measured in tens of seconds rather than minutes. The drug is supplied in 1-mg ampules and is ordinarily diluted in 100 mL of saline to make a concentration of 10 mcg/mL. The median dose of remifentanil that is required to produce loss of consciousness when administered over 2 minutes is 12 mcg/kg; at doses ≤5 mcg/kg, no subjects lost consciousness. It has been recommended that dosing should be calculated on lean body mass and reduced by as much as 50% to 70% in the elderly. Remifentanil, therefore, appears to be very easily titrated. Muscle rigidity has not been observed with infusions up to 0.5 mcg/kg/minute or bolus doses of 25 to 200 mcg. Anecdotally, remifentanil infusion appears to attenuate both the gag reflex and laryngeal reflexes, and can facilitate airway anesthesia. It may be particularly useful in patients with hyperactive gag reflexes, and in the presence of excess secretions, remifentanil may be an invaluable adjunct in awake intubation. Remifentanil may prove to be an exception to the general rule that sedatives cannot or should not be used to compensate for poor regional anesthesia of the airway.

Dexmedetomidine is an alpha-2 agonist that is indicated for the induction of general anesthesia and performance of sedation. It has virtually no respiratory depressant functions, although it may produce profound bradycardia. Infusion by itself and in combination with ketamine has been used for awake fiberoptic intubation. Dexmedetomidine may be a desirable drug for use with fiberoptic intubation, but experience is limited.

Agent selection depends on the clinical situation, medication availability, and familiarity of the sedating professional with the medication. In general, it is best to achieve sedation for airway examination by the same methods used for other procedures so the airway manager is using those agents with which he or she is most familiar and in similar doses.

All agents classified as sedative hypnotics (e.g., benzodiazepines, barbiturates, propofol, and, to some extent, etomidate) cause respiratory depression in a dose-dependent fashion, as do the opioids such as fentanyl and morphine, particularly when use in conjunction with sedative hypnotic agents. Patients with borderline ventilatory drive or barely compensated respiratory failure may be rendered apnoeic by relatively small doses of these agents. Sedative and opioid analgesic agents also produce some degree of muscle relaxation. Patients with upper airway obstruction may become totally obstructed if these agents cause any loss of upper airway muscle tone, and the operator should always be prepared to proceed directly to a surgical airway when sedation and local anesthesia are undertaken on a patient with partial or impending airway obstruction (see Chapter 7).

Levels of sedation lighter than deep general anesthesia are associated with increased intubation difficulty and failure rates. In addition, deep general anesthesia defeats the fundamental purposes of an awake approach (i.e., the maintenance of spontaneous ventilation and active airway protection while one explores alternatives to induction and paralysis).

Ketamine is a dissociative agent and, in doses exceeding 1 mg/kg IV, has respiratory and cardiovascular depressant properties. It may also sensitize the larynx to laryngospasm in the face of laryngeal inflammatory disorders. However, in low to moderate doses, it stimulates respiration, causes mild elevation in heart rate and blood pressure, and maintains muscle tone. Thus, on balance, in the setting of an airway emergency, it may be the best agent to choose to enable the patient to tolerate the evaluation and to continue breathing. The method is to titrate the ketamine in 10- to 20-mg aliquots IV until the patient will tolerate an awake look. The patient may be dissociated but ordinarily will continue to breathe spontaneously and maintain patency of the airway. Some authors advocate a combination of ketamine and propofol drawn up in the same syringe to make a concentration of 5 mg/mL of each (5 mL of 10 mg/mL ketamine plus 5 mL of 10 mg/mL of propofol in a 10-mL syringe) titrated 1 to 2 mL at a time. Although this method administers two agents in a fixed combination, it appears to be effective and safe, and the two drugs are compatible in the same syringe. Alternatives include balanced use of a benzodiazepine (e.g., midazolam) and an opioid (e.g., fentanyl), intravenously titrated etomidate, or other agents used for painful, stimulating procedures. All agents require continuous vigilance with respect to airway patency and adequacy of ventilation.

Local Anesthesia Techniques

Local anesthesia of the airway may be produced topically, by injection, or by combining these two techniques. The selection of a local anesthetic agent will depend on the properties of the agent and how it is supplied (concentration and preparation—aqueous, gel, or ointment). Although the provision of profound local anesthesia in a highly cooperative patient may enable the airway to be visualized and the trachea to be intubated even without sedation, significant systemic sedation will almost always be necessary in the emergency setting.

Determination of the maximum safe dose of local anesthetic agents applied topically to the mucous membrane of the airway is difficult and must take into account the method of topical administration. Traditional dosage guidelines may be excessively conservative when some or all of the drug is administered by aerosol or atomizer inhalation based on the available evidence, with respect to serum levels and toxicity occurrences. However, caution must be exercised, and a precalculated dose should not be exceeded. As always, clinical judgment is required, and meticulous attention to detail should be employed when lidocaine is applied to the airway such that effective anesthesia is achieved without producing toxicity.

The Nose

Topical anesthesia with vasoconstriction is the technique of choice for the nose.

· Using bayonet nasal forceps, place an agent-soaked cotton ball along the floor of the nose toward the back of the inferior turbinate (see Fig. 4-1). Place a second ball just anterior to that, another up against the front of the middle turbinate, and a final one in the vestibule of the nose. It is advisable to place a suture through the cotton balls before placing them. The suture facilitates easy retrieval. Alternatively, surgical patties (strings already attached) or nasal tampons can be used. Some prefer to place a dry nasal Xomed or Merocel wick along the floor of the nose and then inject the agent through a plastic IV cannula along the length of the wick, leaving the soaked wick in place for 10 minutes.

Figure 8-1De Vilbiss Atomizer.

· Adequate topical anesthesia of the dried upper airway can often be achieved by nebulizing a mixture of 4 cc of 4% lidocaine with 1 cc of 1% phenylephrine. This procedure typically takes 10 to 15 minutes, though, and may still require some augmentation by topical spray during the procedure. Note that this approach will administer 160 mg of lidocaine topically, so it must be dose adjusted for small adults and children (toxic dose of lidocaine is 4 mg/kg).

· Alternatively, one may elect to use a DeVilbiss atomizer (Fig. 8-1) or a MAD (Fig. 8-2) to atomize the agent into the nostril while asking the patient to sniff. Atomization produces larger droplets than nebulization. The result is that more of the medication rains out in the upper airway with atomizers than nebulizers, producing a denser block.

Figure 8-2Mucosal Atomization Device (MAD). The syringe forces the local anesthetic solution through the atomizing tip, resulting in a very fine mist, which can be synchronized with the patient's inspiration.

· Vasoconstriction is probably important. Not only does it enlarge nasal passageways, but it may also reduce the risk of mucosal damage and bleeding and enhance the effectiveness of the topical block. Phenylephrine (Neosynephrine) 0.25% solution, or oxymetazoline (Afrin) sprayed and sniffed into the nostrils 2 to 3 minutes before the local anesthetic agent is applied is effective. Alternatively, one can prepare tetracaine 0.45% with epinephrine 1:25,000 (40 mcg/mL) or use 4% cocaine (40 mg/mL) applied by either of the previous methods. The maximum safe dose of tetracaine is 50 to 80 mg; for cocaine, 1 to 3 mg/kg, although toxic reactions have been reported with as little as 20 to 30 mg.

· Virtually all local anesthetic agents are effective when used topically in the nose. However, cocaine 4% and tetracaine 0.45% are particularly effective because of their ability to deeply penetrate tissues and eliminate the deep pressure-type pain commonly associated with inserting devices through the nose. Lidocaine is effective, particularly the 4% aqueous solution (discussed previously), although it tends to cause an intense burning dysesthesia when applied and produces less deep anesthesia, and at 40 mg/mL, toxicity can occur as the volume increases. Most consider 3 to 4 mg/kg applied to a mucosal surface to be a safe maximum dose for lidocaine.

The Mouth

Topical anesthesia of the oral cavity reduces the discomfort generated by grasping the tongue with gauze and pulling it forward to control it and draw the epiglottis forward during a procedure such as bronchoscopic intubation. Secretion of saliva can be eliminated by using an antimuscarinic agent such as glycopyrrolate (Robinul) (0.01 mg/kg intramuscularly or IV; usual adult dose 0.4–0.8 mg). This approach will enhance the block of the oral cavity, tongue, oropharynx, and hypopharynx by permitting superior penetration of the local anesthetic agent. If there is sufficient time (20 minutes is required for this medication to effectively dry the oropharyngeal secretions), it is always advisable to administer glycopyrrolate as part of the local anesthesia of the upper airway.

· The mouth is best anesthetized topically by having the patient gargle and swish with a 4% aqueous solution of lidocaine. The gargling augments the anesthesia of the oro- and hypopharynx.

· An atomizer can also be used to spray the structures of the oral cavity.

The Oropharynx and Hypopharynx

Begin by having the patient gargle, swish, and then spit out 30 mL of 4% lidocaine. For the most part, the sensory supply of the oro- and hypopharyngeal areas is via the glossopharyngeal nerve (see Chapter 4). The best way to achieve local anesthesia of these areas that is sufficiently dense to permit laryngoscopy or awake intubation is to use a technique that blocks this nerve at the base of the palatopharyngeal arch (posterior tonsillar pillar; see Fig. 4-4). Two techniques are commonly used:

· A 23-gauge angled tonsillar needle with 1 cm of exposed needle tip is inserted 0.5 cm behind the midpoint of the posterior tonsillar pillar and directed laterally and slightly posteriorly (Fig. 8-3). Two cc of 2% lidocaine is then deposited following a negative aspiration test. Although this block can be effective, it is not widely used because of the proximity of the carotid artery. A risk of carotid injection up to 5% has been noted.

· A safer way is to use a topical technique. The oral cavity and the pharynx must be thoroughly dry for any topical technique to work. Put 5 mL of 5% lidocaine ointment on the end of a tongue depressor. Have the patient sitting erect and pull the tongue out using gauze. Apply the lidocaine ointment as far back on the base of the tongue as possible using the tongue depressor, as one would apply butter or jam to a piece of toast. Put the tongue back in the mouth and wait 15 minutes. The ointment will liquefy as it warms and will run into the area at the base of the palatopharyngeal arch, penetrating the mucosa to reach the glossopharyngeal nerve. It will also run into the valleculae and pyriform recesses to block the superior branch of the internal laryngeal nerve, producing laryngeal anesthesia.

Figure 8-3Glossopharyngeal Nerve Block: insertion point for a 23-gauge angled tonsillar needle.

The Larynx

The drying imperative does not apply to the larynx. Topical local anesthesia of this structure can be provided using a manual spray device, an atomizer, or a nebulizer to spray 4 to 6 mL of 4% lidocaine aqueous. Alternatively, one can block the superior laryngeal branch of the vagus nerve (see Fig. 4-6):

· The internal branch of the superior laryngeal nerve can be blocked as it runs just deep to the mucosa in the pyriform recess using Jackson forceps to hold a cotton pledget soaked in 4% lidocaine against the mucosa for about 1 minute (Fig. 8-4).

· This block can also be performed using an external approach to the nerve as it perforates the thyrohyoid membrane just below the greater cornu of the hyoid bone. A 21- to 25-gauge needle is passed medially through skin to contact the hyoid bone as posteriorly as possible. The needle is then walked caudad off the hyoid. Resistance may be appreciated as the thyrohyoid membrane is perforated. Following aspiration to rule out entry into the pharyngeal lumen or a vessel, 3 cc 2% lidocaine can be injected. If the hyoid cannot be palpated or if palpation produces undue patient discomfort, then the thyroid cartilage can be used as a landmark. The needle is then walked cephalad from a point on the thyroid cartilage about one-third of the distance from the midline to the greater cornu. Complications again include intra-arterial injection, hematoma, and airway distortion.

Figure 8-4Use of Jackson Cross-over Forceps to Perform a Transmucosal Superior Laryngeal Nerve Block. A cotton pledget, soaked in 4% lidocaine, is held against the mucosa for about 1 minute.

The Trachea

The trachea is best anesthetized topically. Again, drying beforehand is unnecessary. Local anesthetic agent can be sprayed into the trachea using a handheld spraying device, an atomizer, a fiberoptic scope with a working channel, or a nebulizer.

· Tracheal and laryngeal anesthesia can be produced by puncturing the cricothyroid membrane and injecting local anesthetic agent directly into the trachea. A 5-mL syringe containing 3 mL of 4% lidocaine aqueous is attached to a 20-gauge IV catheter over a needle device. It may be helpful to cut the plastic cannula to about 1.5 cm in length to minimize tracheal stimulation and coughing. A small area of skin is anesthetized over the cricothyroid membrane using a 25- to 27-gauge needle TB or insulin syringe to create a wheal. The needle/IV cannula/syringe combination is then inserted into the trachea through the wheal, aspirating for air during insertion. Once the air column is entered, the cut plastic cannula is threaded in over the needle, and the needle is discarded. The lidocaine is injected at end exhalation with the subsequent inspiration and cough facilitating downward and upward spread of the anesthetic, reaching the cords in 95% of cases.

Summary

· Topical anesthesia of the mouth, oropharynx, and hypopharynx will not be fully successful unless the mucous membranes are first dried by the administration of glycopyrrolate.

· An awake look in the context of a difficult airway is primarily accomplished by using IV agents, supplemented by local anesthetic agents. Titrate ketamine or other appropriate sedation agents as for sedation/analgesia for a painful procedure.

· Use benzodiazepines, propofol, and opioids with extreme caution in patients with impending airway obstruction.

Evidence

1. Is there any evidence for the use of ketamine and propofol together? The combination of ketamine and propofol for procedural sedation is a relatively new idea. The anesthesia literature (1,2,3) describes how this combination is used.

2. What are the pharmacodynamics of local anesthetic agents? The physicochemical characteristics of the local anesthetic agents define their clinical behavior, such as their onset time, potency, and duration of action. Detailed descriptions of these agents and their properties are found in the literature (4,5,6,7).

3. Does cocaine cause 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 (8). It is important to realize that medically administered cocaine to produce nasal vasoconstriction has produced similar complications (9,10,11).

4. What is the greatest risk when I am doing an injection glossopharyngeal block? Mongan and Culling (12) described the inadvertent intracarotid injection of a local anesthetic agent during an attempted glossopharyngeal block followed by an immediate seizure.

5. Can local anesthesia of the upper airway cause airway obstruction? Extensive clinical experience with lidocaine has shown it to be an effective topical agent for airway anesthesia and to have a wide margin of safety. However, in the presence of pre-existing airway compromise, topical anesthesia and instrumentation of the airway can be associated with complete airway obstruction, probably due in part to laryngospasm in response to the stimulation of the irritated airway. Whenever one applies topical anesthesia or performs instrumentation of an inflamed, compromised airway, one must be prepared to perform a surgical airway. In certain cases, an awake cricothyrotomy or tracheostomy under local anesthesia may be preferable (13,14,15).

References

1. Mortero RF, Clark LD, Tolan MM, et al. The effects of small dose ketamine on propofol sedation: respiration, postoperative mood, perception, cognition and pain. Anesth Analg 2001;92:1465–1469.

2. Badrinath S, Avrramov MN, Shadrick M, et al. The use of a ketamine-propofol combination during monitored anesthesia care. Anesth Analg 2000;90:858–862.

3. Frey K, Sukhani R, Pawlowski J, et al. Propofol versus propofol-ketamine sedation for retrobulbar nerve block: comparison of sedation quality, intraocular pressure changes, and recovery profiles. Anesth Analg 1999;89:317–321.

4. Cathrall W, Mackie K. Local anesthetics. In: Hardman JC, Linbird LE, Molinoff PS, et al., eds. Goodman and Gilman's the pharmacological basis of therapeutics, 9th ed. New York: McGraw-Hill; 1996:331–347.

5. Ritchie JM, Greene NM. Local anesthetics. In: Gilman AG, Goodman LS, Oilman A, eds. Goodman and Gilman's the pharmacological basis of theraputics, 6th ed. New York: Macmillan; 1980:300–320.

6. Lewin NA, Goldfrank LR, Weisman RS. Cocaine. In: Goldfrank LR, Weisman RS, Flomenbaum NE, et al., eds. Goldfrank's toxicologic emergencies, 3rd ed. Norwalk, CT: Appleton-Century-Crofts; 1986:477–485.

7. Morris IR. Pharmacologic aids to intubation and the rapid sequence induction. Emerg Med Clin North Am 1988;6:753–768.

8. 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.

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

10. 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.

11. 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.

12. Mongan PD, Culling RD. Rapid oral anesthesia for awake intubation. J Clin Anesth 1992;4:101–105.

13. Ho AMH, Chung DC, To EWH, et al. Total airway obstruction during local anesthesia in a non-sedated patient with a compromised airway. Can J Anesth 2004;51(8):838–841.

14. Wong DT, McGuire GP. Management choices for the difficult airway [author reply]. Can J Anesth 2003;50(6):624.

15. Mason RA, Fielder CP. The obstructed airway in head and neck surgery [editorial]. Anaesthesia 1999;54:625–628.



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