Posted by headnecksurgery on January 11, 2009
Local Anesthetic Agents
Local anesthetic agents are weak bases that inhibit nerve conduction by crossing cell membranes and intracellularly blocking electrically excitable sodium channels. Because the cationic form does not readily cross the cell membrane, tissue acidosis renders local anesthetic agents ineffective, and the compounds do not produce anesthesia if injected into abscesses or areas of cellulitis. Local anesthetics tend to be 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. They are further subdivided on the basis of the type of linkage between the benzoic acid moiety and the hydrocarbon chain. Anilide anesthetics (lidocaine, mepivacaine, bupivacaine, and ropivacaine) contain an aminoamide linkage, whereas an aminoester bond characterizes ester anesthetics (cocaine, tetracaine, and benzocaine).
The type of bond dictates the site of metabolism and route of excretion of both classifications of local anesthetic. Hepatic microsomal enzyme systems degrade the anilides into metabolites that possess varying degrees of anesthetic potency. This process can be profoundly inhibited by cimetidine, which blocks microsomal activity, or by propranolol, which reduces delivery of the drug to the liver through a decrease in hepatic blood flow. Plasma cholinesterase metabolizes the aminoester drugs. This process is much more rapid than hepatic metabolism and can be inhibited by previous administration of anticholinesterase drugs, such as neostigmine. All local anesthetics should be used only after the practitioner calculates the safe total dose of the anesthetic for the patient. This amount of drug can be prepared, and no more anesthetic is given once this amount is administered.
The aminoamide local anesthetic agents, such as lidocaine, are weak vasodilators that necessitate the addition of a dilute solution of epinephrine or phenylephrine to aid in vasoconstriction. Lidocaine is used as both a topical and an injectable local anesthetic. Four percent 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 dose is 5 mg/kg without epinephrine or phenylephrine and 7 mg/kg with a vasoconstrictive agent. 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. The total safe dose of epinephrine in operations on adults is 200 µg. Toxic levels of epinephrine cause hypertension, arrhythmia, and tachycardia. The arrhythmogenic effects of these catecholamines can be exaggerated by concurrent use of inhaled anesthetics, particularly halothane, or pancuronium. Mepivacaine has an efficacy and toxicity profile similar to that of lidocaine but diffuses more readily through tissues and has a longer half-life.
The remaining aminoamide local anesthetic agents are less commonly used during otorhinolaryngologic surgery. Because of its long duration of action, bupivacaine 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 3 mg/kg when injected alone and 4 mg/kg when used with epinephrine. Much lower doses can cause toxicity when administered through the intravenous, intrapleural, or intrathecal route. Ropivacaine is a newer agent that has similar efficacy to bupivacaine but is less toxic and produces less motor block for the same degree of sensory block.
Cocaine is unique among the topical anesthetics because in addition to being an excellent topical anesthetic, it is also 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 because it is highly addictive and is one of the most abused drugs. For this reason, cocaine use is limited in clinical practice to the mucous membranes of the head and neck. Studies have failed to substantiate the claim that cocaine is irreplaceable in otolaryngology. Combinations of lidocaine and epinephrine, phenylephrine, or oxymetazoline have been shown to be as efficacious as cocaine for a number of purposes, so many otolaryngologists do not use cocaine at all. Cocaine is commonly used as 4% solution for direct application to mucous membranes. The onset of action is quick (5 to 10 minutes), and the duration of action is as long as 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 be fatal. The total dose of cocaine applied to the mucosa should be limited to 3 mg/kg. Severe or even fatal toxicity from cocaine can be caused by either central nervous system or cardiovascular effects. Care should be taken in administering either epinephrine or cocaine to patients with hypertension, history of arrhythmia, thyrotoxicosis, or coronary artery disease. Tetracaine is another excellent topical anesthetic agent and is the best topical anesthetic for ophthalmologic procedures. Although it has 10 times the potency of cocaine, tetracaine lacks the vasoconstrictor effect of that drug. Benzocaine produces more profound topical anesthesia than does tetracaine and does so with less toxicity. This drug often is used for topical application to the upper aerodigestive tract.
Local anesthetic techniques are used in otolaryngology in situations, such as cosmetic facial surgery, in which distortion of the tissue is undesirable. For this reason, using smaller volumes of local anesthetic while accomplishing analgesia is the goal. Infiltration of local anesthetic around the peripheral nerve that supplies the surgical field with sensation often is desired. 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 thorough understanding of the anatomic features of the head and neck. The technique involves use of a 25-gauge needle to infiltrate lidocaine or bupivacaine around sensory nerve branches as they exit the facial skeleton. Care must be taken to avoid direct intravascular injection because unintentional injection of local anesthetic into the vertebral or carotid artery can precipitate a seizure. The practitioner always should withdraw the plunger before injection of local anesthetic. Careful use of this technique rarely causes complications.
Procedures on the face performed with local anesthesia are begun after branches of the fifth cranial nerve are blocked. Blocking the supraorbital and supratrochlear nerves with 1 to 3 mL 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 often can be palpated. The supratrochlear nerve is about 1 cm more medial. Anesthesia of the external nose necessitates blocking the bilateral anterior ethmoidal nerves and infratrochlear nerves. This is accomplished with either transcutaneous or submucosal injection at the junction of the upper lateral cartilage and the nasal bones laterally that is extended superiorly between the medial canthus and the nasal dorsum.
The maxillary nerve (V2) 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. This block is not in common use; procedures that necessitate such extensive anesthesia of the midface are more often performed with general anesthesia. Blockade of the major terminal branches of the maxillary nerve is more commonly used.
Infraorbital nerve block anesthetizes the maxillary incisors, cuspids and bicuspids, associated gingiva, the lower eyelid, anterior cheek, and the upper lip. Less than 3 mL of solution is needed. The nerve is reached with either an external or a sublabial approach. The nerve is in line with the pupil and about 1 cm below the infraorbital rim. The palate can be anesthetized by means of 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. Care must be taken because 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 posteriorly 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 about 1 cm above the occlusal surface of the posterior molars at the anterior-posterior level of the coronoid notch. With the 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 the lingual nerve 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 cranial nerve V3 is the mental nerve. This blockade is accomplished with 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 by remembering that it is in line with the pupil. This technique anesthetizes the lower lip, gingiva, and teeth from the bicuspids to the midline.
Anesthesia of the neck, inferior and posterior auricle, and scalp can be accomplished by means of blockade of the cervical plexus. 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 done with care to avoid injection into the vertebral artery, and spread to involve the phrenic nerve is likely. 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 is used to facilitate endoscopic procedures performed with local anesthesia and is used to allow endoscopic intubation of patients for whom topical anesthesia is difficult.