Pain and Anxiety Control in Surgical Practice


Virtually all oral surgery procedures produce pain, and for most patients the prospects of having surgery provoke some degree of anxiety. Therefore it is incumbent upon those performing oral surgery to master techniques that will control perioperative pain and anxiety. For most routine oral surgical procedures, local anesthesia is sufficient to manage pain produced during surgery and for the early postoperative period. Anxiety control, on the other hand, is a more complex topic. Patients may or may not require pharmacologic control. Most patients are adequately managed using nonpharmacologic behavioral techniques. However, some form of drug-mediated sedation is often useful or required for patients with higher levels of presurgical anxiety or for procedures known to cause intraoperative anxiety. This chapter focuses on the use of local anesthesia for routine oral surgery and limits it coverage of anxiety control to nitrous oxide sedation. The topics of local anesthesia and sedation for dental care are far more comprehensively covered in other textbooks.

Local Anesthesia

The ability to locally anesthetize a specific part of the body is one of the marvels of pharmacology. It is hard to imagine the modern practice of dentistry without the availability of local anesthetics (LAs). The dental pulp and soft tissues adjacent to teeth are highly sensitive to stimulation of all forms, including pain-provoking stimuli. Thus profound local anesthesia is mandatory to properly perform oral surgery on an awake patient.

A large number of LAs are available for use by dental practitioners. However, like most medications, those administering drugs find it optimal to limit the number of different forms of a drug to produce a similar effect. This allows the clinician to truly master the use of the category of drug they select to administer, becoming completely familiar with the drug's chemistry, mechanism of action, and clinical pharmacodynamics. Practitioners choosing to limit the number of different versions of a category of drug are then able to focus on just those drugs. This gives them the opportunity to gain valuable clinical experience with the use of these drugs, enabling them to recognize usual and unusual patient reactions and more easily stay abreast of new knowledge related to these drugs. For this reason, this chapter limits its coverage to only six specific LAs. Other LAs are available throughout the world that are efficacious, and other references are available to provide detailed information about them.

Mechanism of Action

LAs are, by definition, designed to block the function of sensory nerves, although they are also able to inhibit motor nerves and other nerve tissues. To understand the mechanism of action of LAs, one must recall how nerve fibers transmit electrical impulses. In the case of sensory nerves, when the peripheral nerve ending or nerve trunk is sufficiently stimulated, the resting potential of the nerve membrane is triggered to depolarize by a change in membrane permeability that allows the shift of sodium ions across the membrane into the axoplasm. Initially, a slow depolarization occurs; however, once the negative transmembrane potential decreases to the point of the firing threshold, rapid depolarization occurs. Local currents within the axon help propagate the impulse down the axon, triggering rapid depolarization along the path to the cell body and central nervous system (CNS).

LAs primarily function by raising the membrane firing threshold necessary to trigger or propagate an electric impulse. LAs also produce local anesthesia by affecting sensory receptors and nerve membranes in other ways. The end result is that the nerve membrane remains in a polarized state unable to conduct impulses and not transmit otherwise painful sensations.

Pharmacology

The chemistry of various LAs directly affects the pharmacologic properties of each drug. The LAs discussed in this section are all tertiary amines and classified as amino amides, making them relatively resistant to hydrolysis. LAs tend to work best at a neutral pH. The pH of LAs without vasoconstrictors is about 6.5. Manufacturers lower the pH of LAs when vasoconstrictive agents such as epinephrine are added to inhibit the oxidation of the vasoconstrictor. The acidification of the LA produces the “burning” sensation patients can experience during injection. Another clinical effect related to local anesthetic pH is the tendency for LAs to be less effective when injected into an area of inflammation/infection. This happens because of the acidic nature of inflamed tissue that interferes with local anesthetic effectiveness.

LAs differ in their ability to bind to proteins and in their lipid solubility; they also come in varying concentrations. These factors affect their speed of onset and duration of action. When used for oral surgery the onset of action is also affected by the proximity of the injected deposition of the local anesthetic to the target nerve. The less the distance the drug needs to diffuse to reach the nerve, the faster the onset. The duration of action is affected by the amount of drug deposited and the vascularity of the tissue in the area of the injection. The more drug deposited and the less drug removed by local blood vessels, the longer the duration of action. Vasoconstrictors are added to LAs to dampen the effects of local vessels on drug removal, thereby prolonging the drug's duration.

The pharmacology of the various local anesthetic solutions that are used should be kept in mind so that they can be administered properly. Table 6.1 summarizes commonly used LAs and the expected duration of complete anesthesia. The surgeon must remember that pulpal anesthesia of maxillary teeth after local infiltration lasts a much shorter time compared with pulpal anesthesia of mandibular teeth after block anesthesia. In addition, pulpal anesthesia disappears 60 to 90 minutes before soft tissue anesthesia. Therefore it is common for the patient to have lip anesthesia but to have regained pulpal sensation and so may experience pain.

TABLE 6.1
Duration of Anesthesia
Local Anesthetic Maxillary Teeth Mandibular Teeth Soft Tissue
Group 1 a 10–20 min 40–60 min 2–3 h
Group 2 b 50–60 min 90–100 min 3–4 h
Group 3 c 60–90 min 3 h 4–9 h

a Group 1—local anesthetics without vasoconstrictors: mepivacaine 3%, prilocaine 4%.

b Group 2—local anesthetics with vasoconstrictors: lidocaine 2% with 1:50,000 or 1:100,000 epinephrine, mepivacaine 2% with 1:20,000 levonordefrin, prilocaine 4% with 1:400,000 epinephrine, articaine 4% with 1:100,000 epinephrine.

c Group 3—long-acting local anesthetics: bupivacaine 0.5% with 1:200,000 epinephrine, etidocaine 1.5% with 1:200,000 epinephrine.

Toxic Reactions

Only a certain amount of local anesthetic can be safely used in a given patient. To provide anesthesia for multiple tooth extractions, it may be necessary to inject multiple cartridges of the local anesthetic. Thus it is important to know how many cartridges of a given local anesthetic solution can be administered safely. Table 6.2 summarizes (in two different ways) the maximum amounts of local anesthetic that can be used. First, each local anesthetic has a recommended maximum dose based on milligrams per kilogram (mg/kg). The second column in Table 6.2 indicates the number of cartridges that can safely be used on a healthy 154-lb (70-kg) adult. Rarely is it necessary to exceed this dose, even in patients heavier than 154 lb. Patients who are smaller, especially children, should be given proportionally less local anesthetic. A common risky situation involving local anesthetic overdose is the administration of 3% mepivacaine (Carbocaine) to a small child. For a child who weighs 44 lb (20 kg), the recommended maximum amount of mepivacaine is 100 mg. If the child is given two cartridges of 1.8 mL each, the dose totals 108 mg. Therefore a third cartridge of 3% mepivacaine should not be administered. As with any drug, the smallest amount of local anesthetic solution sufficient to provide profound anesthesia is the proper amount.

TABLE 6.2
Recommended Maximum Local Anesthetic Doses
Drug/Solution Maximum Amount (mg/kg) Number of Cartridges for 70-kg (154-lb) Adult Number of Cartridges for 20-kg (44-lb) Child
Lidocaine 2% with 1 : 100,000 epinephrine 5.0 10 3.0
Mepivacaine 2% with 1 : 20,000 levonordefrin 5.0 10 3.0
Mepivacaine 3% (no vasoconstrictor) 5.0 6 2.0
Prilocaine 4% with 1 : 200,000 epinephrine 5.0 6 2.0
Articaine 4% with 1 : 100,000 epinephrine 7.0 6 1.5
Bupivacaine 0.5% with 1 : 200,000 epinephrine 1.5 10 3.0
Etidocaine 1.5% with 1 : 200,000 epinephrine 8.0 15 5.0

LAs can affect all types of nerves including those controlling the myocardium and peripheral blood vessels. In addition, because LAs can cross the blood-brain barrier, they can also affect CNS tissue. Excessive levels of LAs cause myocardial depression. This may reduce cardiac output and allow abnormal rhythms to occur. When at toxic levels LAs affect the peripheral blood vessels by relaxing smooth muscles responsible for maintaining normal vascular tone; this leads to hypotension. In the CNS, toxic levels of LAs have paradoxical effects. At the lower end of toxic levels LAs can produce CNS signs and symptoms of depression and have anticonvulsant properties. However, as the serum concentration rises to higher toxic levels, a preconvulsant state is produced that may lead to convulsions.

Vasoconstrictors

The two most common vasoconstrictors added to LAs used for dental surgery are epinephrine and levonordefrin. LAs used for oral surgery have varying concentrations of these two drugs. Epinephrine is added to all the LAs discussed in this chapter except mepivacaine. Mepivacaine is available in two forms; 3% mepivacaine used for dentistry contains no vasoconstrictor, whereas the 2% formulation of mepivacaine has levonordefrin in a 1/20,000 concentration.

Both epinephrine and levonordefrin prolong the duration of local anesthesia by producing local vasoconstriction. They also can promote local hemostasis through their vasoconstrictive effects on capillary beds. Epinephrine and levonordefrin have similar effects on other parts of the cardiovascular system, producing an increase in heart rate, myocardial contractility, and blood pressure. The cardiac effects increase myocardial oxygen consumption and may provoke dysrhythmias. Therefore techniques to limit the amount of these vasoconstrictors are part of the standard protocol of their administration; namely, aspirating before depositing the anesthetic in tissues with sizable blood vessels and limiting the total amount of local anesthetic used. This becomes even more important for patients with preexisting cardiovascular disorders such as coronary artery disease or dysrhythmic tendencies and in patients with poorly controlled hypertension. Yet it must be kept in mind that an inadequate degree or duration of local anesthesia exposes patients to intraoperative pain sensations that will then stimulate endogenous catecholamine release. Therefore guidelines exist about the use of vasoconstrictor-containing LAs to try to balance the need for profound anesthesia for the duration of a procedure with the requirement to avoid potentially dangerous side effects of vasoconstrictors.

Modulation of Injection Discomfort

In many clinical circumstances, patients are more fearful of the local anesthetic injection than of the surgical procedure. Although there are ongoing studies investigating the efficacy of buffered LAs to lessen the pain produced because of their acidity, there is little to counteract the burning or heavy pressure sensation patients feel while LAs are being deposited in the tissues when commonly available anesthetic syringes are in use. However, there are means of lessening the discomfort of the anesthetic needle piercing the mucosa. Local anesthetic needles are sharp and have a small diameter; therefore, when inserted properly, they cause relatively little discomfort. Many practitioners choose to use topical anesthesia before needle insertion to further minimize the discomfort of the injection. Benzocaine has pharmacologic properties that make it a useful topical anesthetic for oral mucosa. It has a very rapid onset of action (typically <1 minute) and an extremely low risk of causing unwanted side effects. When applied to dried mucosa it can eliminate the discomfort of needle insertion within 60 seconds. However, benzocaine does not penetrate deep enough to eliminate the discomfort of anesthetic deposition.

Other approaches to lessening the pain of a local anesthetic injection include lowering the rate of injection, prewarming anesthetic cartridges, and using distraction techniques such as wiggling adjacent tissue like the cheek or talking to the patient about topics unrelated to their surgery during the injection. For some patients, nitrous oxide sedation may be necessary prior to local anesthetic injection (discussed later in this chapter).

Relevant Anatomy

Profound local anesthesia is needed if the tooth is to be removed without causing sharp pain for the patient; therefore it is essential that the surgeon remember the precise innervations of all teeth and surrounding soft tissue, as well as the kinds of injection necessary to anesthetize those nerves completely. Table 6.3 summarizes the sensory innervation of teeth and the surrounding tissue. Figs. 6.1 to 6.4 show the primary nerves relevant to local anesthesia for dentoalveolar surgery.

TABLE 6.3
Sensory Innervation of Jaws
Nerve Teeth Soft Tissue
Inferior alveolar nerve All mandibular teeth Buccal soft tissue of premolars, canines, and incisors
Lingual nerve None Lingual soft tissue of all teeth
Long buccal nerve None Buccal soft tissue of molars and the second premolar
Anterior superior alveolar nerve Maxillary incisors and canine teeth Buccal soft tissue of incisors and canines
Middle superior alveolar nerve Maxillary premolars and a portion of the first molar tooth Buccal soft tissue of premolars
Posterior superior alveolar nerve Maxillary molars except for a portion of the first molar tooth Buccal soft tissue of molars
Greater palatine nerve None Lingual soft tissue of molars and premolars
Nasopalatine nerve None Lingual soft tissue of incisors and canines

Fig. 6.1, Superior alveolar nerve branches innervating maxillary teeth and adjacent labiobuccal soft tissues.

Fig. 6.2, Greater palatine and incisive nerves innervating soft tissue over the hard palate.

Fig. 6.3, Inferior alveolar nerve innervating mandibular teeth and soft tissues in distribution of the mental nerve.

Fig. 6.4, Lingual and mylohyoid nerves innervating tongue and soft tissues of the floor of the mouth.

When anesthetizing a maxillary tooth for extraction, the surgeon should anesthetize adjacent teeth as well. During the extraction process, adjacent teeth are usually subjected to some pressure, which may be sufficient to cause pain. This is also true for mandibular extractions, but the mandibular block injection usually produces sufficient anesthesia to adjacent teeth.

Dense local anesthesia results in the loss of all pain, temperature, and touch sensations, but it does not anesthetize the proprioceptive fibers of the involved nerves. Thus, during an extraction, the patient feels a sensation of pressure, especially when the force is substantial. The surgeon must therefore remember that the patient will need to distinguish between sharp pain and the dull, albeit intense, feeling of pressure when determining the adequacy of anesthesia. It is often difficult to make this distinction.

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