18: Management of Pain and Anxiety

Management of Pain and Anxiety

Gwen I. Hlava, Todd N. Junge, and the publisher acknowledge the past contributions of Danielle Leigh Ryan to this chapter.

As clinicians, dental hygienists must be able to manage the client’s pain and anxiety. This requires mastery of head and neck anatomy, physiology, pharmacology, medical emergencies, and clinical technique. Local anesthetic agent administration is within the legal scope of dental hygiene practice in most legal jurisdictions in the United States. This chapter reviews four methods to relieve and manage pain and anxiety: (1) local anesthesia, (2) topical anesthesia, (3) computer-controlled local anesthesia, and (4) nitrous oxide–oxygen conscious sedation.

Characteristics and Physiology of Pain


Pain reactions and pain-reaction thresholds vary from individual to individual and within the same individual from day to day

Pain perception

1. Functional unit—neuron, or nerve cell

2. Types of nerve cells

3. Sensory neuron characteristics (Figure 18-1)

4. Fiber diameter—varies; determines speed of impulse conduction and type of pain perceived

5. Nerve trunk versus ganglia—a nerve trunk is an extremely large bundle of nerve fibers or axons; a ganglion is the site where cell bodies are bundled

Resting nerve cell membrane

Minimal threshold stimulus


1. When a minimal threshold stimulus excites the nerve:

2. Depolarization—the time interval that exists while ionic concentrations are reversing

3. Reversed polarity—the result of a reversal in ionic charges

4. Repolarization—occurs after reversed polarity; the membrane becomes hyperpermeable to K+ and impermeable to Na+; polarity is re-established

5. Action potential—rapid sequence of changes in the membrane potential (negative to positive, and positive back to negative); the stages are:

6. Absolute refractory period—the period during depolarization and reversed polarity when the cell membrane cannot be re-excited

7. Relative refractory period—during repolarization, the nerve cell membrane can be re-excited, but it requires a greater stimulus than the stimulus required for excitation from the resting state

Pain intensity determined by:

Pain reaction—determined by a person’s pain reaction threshold


Definition—all items essential for the administration of a local anesthetic agent

Armamentarium categories

1. Needle

a. Components (Figure 18-2)

b. Composition—stainless steel

c. Gauge (ga)—the diameter of the lumen is indicated by a number

d. Length—measured from hub to the point of bevel

e. Method of sterilization—disposable needles come presterilized, with a security seal

2. Anesthetic cartridge

a. Components (Figure 18-3)

b. Ingredients in the anesthetic solution

c. Method of storage—away from direct sunlight and ultraviolet light, and maintained at room temperature (68°F to 77°F; 20°C to 25°C) or slightly cooler

3. Anesthetic syringe (Figure 18-4)

a. Components

b. Method of syringe sterilization—the bioburden is removed; the syringe is dried, packaged, and sterilized

c. Auxiliary materials—hemostat or cotton pliers; used if the needle breaks

Record keeping and documentation in client dental record

Local Anesthetic Agents

Chemical Structure

Chemical components (Table 18-1)

Allergies related to chemical structure


Definition—the amount of drug capable of causing adverse systemic reactions in normal persons; adverse reactions occur when the rate of drug absorbed is greater than the rate of biotransformation, the body’s ability to metabolize the drug

True toxic reactions occur immediately—the most profound effects of toxic reaction are on the central nervous system (CNS) and the cardiovascular system

Topical Anesthetic

Purpose—reduces the discomfort associated with the initial penetration of the needle through the mucosa

Controversy exists with regard to widespread use

Esters have a greater incidence of allergic reactions and cross-reactivity than amides

Topical agents have indications and contraindications; can interact with other medications; clinicians must always assess for potential allergies, side effects, and adverse effects and take appropriate precautions

Calculating the Amount of Local Anesthetic Drug in an Anesthetic Solution

Maximum recommended dose (MRD)—maximum amount of drug administered that does not produce a toxic reaction

Example of calculations

1. Percentage of the anesthetic drug is the number of grams (g) of drug per 100 milliliters (mL) of solution (e.g., 2 g anesthetic drug/100 mL solution = 2% anesthetic solution). To find the number of milligrams of drug in 1 milliliter of solution, change the grams of drug to milligrams (mg) by multiplying by 1000 (e.g., 2 g drug/100 mL solution × 1000 mg/1 = 2000 mg/100 mL = 20 mg drug/1 mL solution). This calculation determines that 20 mg of anesthetic drug (e.g., lidocaine) are in each milliliter of this anesthetic solution

2. To calculate the number of milligrams of anesthetic drug (e.g., lidocaine) that is administered, multiply the number of milligrams per milliliter of the drug by the number of milliliters of solution administered

3. To compute the MRD of an anesthetic drug in cartridges, divide the MRD in milliliters by the number of milliliters in 1 cartridge (1.8). The MRD of lidocaine 2% is 15 milliliters (15 mL/1.8 mL = 8.3 cartridges)

Vasoconstrictors (Table 18-2)

Definition—one of five ingredients in an anesthetic solution that functions to hold the anesthetic agent in the area where anesthesia is delivered

Description—all vasoconstrictors can be referred to as adrenergic drugs or sympathomimetic amines

Function—hold the local anesthetic agent in the target site of analgesia by producing vasoconstriction; if absent from a local anesthetic agent, vasodilation will occur; the results of vasoconstriction are:

Mode of action—stimulate α-receptors located in the walls of arterioles

1. α-receptors—responsible for arterial constriction

2. β-receptors—responsible for dilation

3. Each type of vasoconstrictor possesses varying degrees of response of both α- and β-activity (see Table 18-2); although epinephrine exhibits the most β-activity, to achieve the same amount of vasoconstriction as epinephrine, the concentration of all other vasoconstrictors must be increased

Biotransformation—metabolism of vasoconstrictors occurs in the bloodstream; the enzyme responsible for biotransformation is monoamine oxidase (MAO); persons taking MAO inhibitors have a decreased ability to metabolize vasoconstrictors

Pressor potency—the ability of a drug to produce vasoconstriction

Vasoconstrictors in solution—unstable; preservative (e.g., sodium bisulfite) is added to prevent oxidation

Toxicity—toxicity resulting from vasoconstrictor overdose is caused by constriction of blood vessels, which raises blood pressure and cardiac rate from β-receptor stimulation

Dosage calculations (maximum recommended dose); for example, epinephrine 1 : 100,000

Jan 1, 2015 | Posted by in Dental Hygiene | Comments Off on 18: Management of Pain and Anxiety
Premium Wordpress Themes by UFO Themes