14: Pain Management

CHAPTER 14 Pain Management

DENTAL PAIN

Pain is sum total of responses (behavioral, emotional, motivational, psychological) to actual or impending tissue damage from noxious stimulus.

• See CD-ROM for Chapter Terms and WebLinks.

A. Types of dental pain:

1. Caused by dental disease or trauma.

2. As result of dental treatment (iatrogenic).

3. After dental treatment.

B. Pain perception:

1. Physioanatomical process by which pain is received and transmitted by neural structures from end organs and pain receptors, through conductive and perceptive mechanisms.

2. Does NOT differ much from person to person, same in MOST healthy persons, but can be affected by both disease and toxic states.

C. Pain reaction:

1. Manifestation of perception of pain that has been perceived by the brain.

2. Determines what a patient will do about the unpleasant experience of pain.

3. Differs a great deal from person to person because of past dental experiences and various factors such as fatigue, stress, fear, apprehension, age, emotional state, education.

D. Pain threshold: tolerance shown to pain; there are differing levels:

1. Hyporeactive: high pain threshold, tolerates pain well, shows little reaction to pain.

2. Hyperreactive: low pain threshold, does NOT tolerate pain well, shows more reaction to pain.

3. However, MOST patients vary between two types depending on factors (discussed earlier).

E. Gate control theory of pain (GCT):

1. Explains unusual phenomenon of pain past specific neural pathway of pain sensation.

2. Specific neuroanatomical pathway carries impulse from site of stimulus to cortex of the brain where it is perceived as pain and then person receives a painful sensation.

3. Thus perception of physical pain is NOT direct result of activation of pain receptor neurons, but instead is modulated by interaction between different neurons.

4. Before pain messages can reach the brain, messages encounter “nerve gates” in spinal cord (sympathetic ganglion [SG]) that open and close depending on a number of factors:

a. When gates are opening, MORE pain messages get through and pain can be intense.

b. When gates close, pain messages are prevented from reaching the brain and pain may NOT even be experienced.

F. Responses to pain:

1. Physiological: increased respiratory rate, increased heart rate (HR), increased blood pressure (BP).

2. Physical: crying out, tapping feet, cold sweat, altered facial expression, white knuckles, inability to sit still.

G. Pain control and dental office:

1. Pain is a major factor that brings patients to dental office, while fear and anxiety about pain are MOST common reasons patients fail to seek dental care; many AVOID dental treatment until forced into office with an emergency.

2. Control of pain and anxiety is therefore essential part of dental practice:

a. To accomplish this objective, various techniques are used, including psychological approaches, local anesthetics of various types, and combinations of sedative and general anesthetic agents.

b. Choice of MOST appropriate modality for particular situation is based on training, knowledge, and experience of clinician; nature, severity, duration of procedure; age and physical and psychological status of patient; level of fear and anxiety; previous responses to pain control procedures.

c. MUST keep “gates closed” to pain messages to control dental pain (see earlier discussion) (No pain, lots of gain!).

3. Important part of stress control protocol, especially in management of patients with cardiovascular disease (CVD).

Anxiety Management

Anxiety is the feeling of apprehension and fear characterized by physical symptoms such as palpitations, sweating, feelings of stress. Anxiety keeps many people from receiving necessary dental treatment because of fear of pain or discomfort. Fear is excessive apprehension or anxiety. Understanding dental fear can help in selecting appropriate methods for alleviating patient discomfort. Anxiety and fear are common occurrences in the dental office and can be managed by a variety of techniques. Sometimes fear can become excessive and involve a phobia, which promotes inaction (failure to seek necessary dental treatment).

A. Etiology of dental anxiety and fear:

1. Anxiety and fear are typically based on past dental experiences.

2. May be based on fearful experiences related by others (friends or family) or portrayed by media.

3. Iatrogenic causes arise from personal experiences with dental situations and personnel (typically during childhood); two greatest dental fears are needles and dental drill.

4. Feeling a loss of control can increase dental anxiety and fear.

B. Treatment of dental anxiety, fear, phobias:

1. Using systemic desensitization (small doses of positive experiences) for highly anxious patients increases tolerance for dental encounters.

2. Explaining procedures thoroughly decreases fear of unknown.

3. Increasing patient control during each treatment session decreases fear of helplessness and increases sense of trust (allow patient to help with suction by holding patient saliva ejector or pick out favorite flavor of topical).

4. Using relaxation techniques in dental environment, includes headphones or other distracters, calming voice, biofeedback, adhering to time schedule.

5. Using pharmacological control of anxiety:

a. Antianxiety premedication, either orally or IV, with benzodiazepines (BZDs), diazepam (Valium), or alprazolam (Xanax); patient will have LESS memory of stressful dental procedures (see Chapter 9, Pharmacology).

b. Topical and/or injected local anesthesia agents can remove pain during dental procedures (discussed later).

c. Sedation with nitrous oxide can give MORE relaxation, increase pain threshold, decrease awareness of time and procedures, increase sense of well-being (discussed later).

d. Posttreatment with antiinflammatories (such as ibuprofen) can reduce inflammation and thus pain, helping with healing (see Chapter 9, Pharmacology).

CLINICAL STUDY

Scenario: A 35-year-old woman has not been to the dentist’s office for 10 years. During her last dental experience, she had two third molars extracted and the local anesthetic initially used did not provide pulpal anesthesia. Repeated injections did not improve the situation but did make her more anxious and uncomfortable, and the extraction proceeded without anesthesia for the patient. Lately her gums have been bleeding and sore. Her husband persuaded her to have a thorough exam and cleaning. After diagnosis of generalized chronic periodontitis, her treatment plan suggests nonsurgical periodontal therapy by quadrant dental hygiene using local anesthesia of the involved regions. On the day of her appointment with the dental hygienist, the patient calls and cancels.

1. What is the major problem confronting the patient?

2. Identify the most effective methods for treating the patient’s condition.

3. What is the difference between fear and a phobia?

1. Anxiety related to past dental experiences is the problem the patient is most likely confronting.

2. First, the patient must visit the dental office to be fully informed about the necessary dental procedures. Next, for site-specific soft tissue anesthesia the hygienist should help patient identify problems that occurred before and explain choices that will decrease likelihood of similar occurrences during dental hygiene treatment. Patient needs to feel in control of situation.

3. Phobia is excessive fear that leads to inaction, such as failure to seek necessary dental treatment, which can be detrimental to a person’s health and well-being.

Sensory Innervation

Peripheral nervous system (PNS) comprises sensory (afferent) nerves that carry sensations of pain to central nervous system (CNS), and motor (efferent) nerves that transmit messages from CNS to muscles and glands. Understanding of sensory nerve anatomy and physiology and action of local anesthetics is essential to pain management. Sensory nerves are afferent nerves that carry sensations of pain to the CNS.

• See Chapters 3, Anatomy, Biochemistry, and Physiology: nervous system anatomy and physiology; 4, Head, Neck, and Dental Anatomy: trigeminal nerve.

A. Anatomy of a nerve:

1. Myelinated nerves (comprise MOST nerves in the body), divided into three zones:

a. Dendrite (free nerve endings): reacts to stimuli in the surrounding tissues.

b. Axon: pipeline that delivers impulses to CNS.

c. Terminal nerve endings (arborization): synapse with CNS nerves.

2. Structure of single nerve fiber: myelin sheath covers axon, composed MAINLY of lipid layers (75%) and protein (20%) (Figure 14-1):

a. Lipid layers: act as barriers to some molecules and as binding sites for lipophilic components of local anesthetics.

b. Proteins: act as channels to allow some ions (Na⁺, K⁺) to pass through nerve membrane.

3. Layers of a nerve:

a. Epineural sheath: outermost layer; NOT a barrier to anesthetics.

b. Epineurium: connective tissue layer; carries fasciculi, blood vessels, and lymphatic vessels; as anesthetic diffuses through epineural sheath and blood vessels, begins to eliminate anesthetic.

c. Perineurium: surrounds the fasciculi; greatest barrier to local anesthetic.

4. Nodes of Ranvier: constrictions 0.5 to 3 mm apart; nerve impulses travel from node to node.

B. Structure of a nerve bundle: MANY peripheral nerves have hundreds to thousands of tightly packed axons in bundles called fasciculi (Figure 14-1).

1. Mantle bundles: outside of nerve bundle, receive anesthetic FIRST; innervate proximal areas (posteriors) and lose anesthetic properties FIRST.

2. Core bundles: inside of a nerve bundle; receive anesthetic last and in lower concentration because of distance from anesthetic source and presence of more blood vessels; innervate distal areas (anterior) and lose anesthetic properties last.

C. Physiology of a nerve:

1. Nonstimulated nerve has Na⁺ ions outside the membrane, K⁺ ions and negative ions inside, and resting potential of −70 mV.

2. Stimulation of nerve is caused by mechanical (instrument in the soft tissue), chemical, thermal, or electrical means; starts depolarization process; permits movement of ions across nerve membrane; electrical potential changes from 50 to 60 mV to +40 mV; as electrical potentials change, impulse moves along nerve from node to node.

3. Repolarization occurs when Na⁺ ions begin to move back across nerve membrane to increase negative potential inside nerve; from stimulation to repolarization, process takes ∼1 msec.

Figure 14-1 Structure of a neuron and relationship with other neuron (and muscle tissue).

(From Bath-Balogh M, Fehrenbach MJ: Illustrated dental embryology and anatomy, ed 2, Philadelphia, 2006, Saunders/Elsevier.)

LOCAL ANESTHESIA

Dental patients can benefit from removal of pain during dental procedure with local anesthesia, as well as hemorrhage control from use of a vasoconstrictor, along with use of topical anesthesia. Can be used alone or with a combination of nitrous oxide sedation, which alone does NOT replace local anesthesia for pain control, since it is an analgesic and not an anesthetic. Local anesthesia administration by dental hygienists is allowed in only some states and usually under the supervision of a dentist.

The CORRECT administration of local anesthesia involves understanding nerve anatomy and physiology, pharmacology, armamentarium, technique, and possible complications. Action of local anesthetic agent depends on chemical structure and pH of the solution and body tissues.

A. Mode of action: a local anesthetic prevents or blocks Na⁺ channel function in neurons.

1. Stabilizes the nerve membrane so that the membrane threshold is elevated to point where depolarization does NOT occur.

2. Thus, Na⁺ channels do NOT open and Na⁺ ion will NOT enter the axon.

3. Depresses all unmyelinated fiber FIRST and larger myelinated fibers last.

4. General order of loss of function (first to last): pain, temperature, touch, proprioception, motor nerve function.

B. Chemical formula of agent (Figure 14-2):

1. Aromatic group (lipophilic [hydrophobic] component): affinity for the lipid portion of the myelin sheath, which helps local anesthetic agent attach to the nerve membrane and block the nerve impulse.

2. Intermediate chain: either ester (−COO−R) or amide (NHCO−R) group; determines mode of biotransformation or metabolism (see later discussion).

3. Amino end (hydrophilic component): makes anesthetic agent injectable; amides dissolve poorly in water and are unstable on exposure to air; therefore hydrochloride (HCl) is added to produce a salt that is MORE soluble and stable.

C. Discussion of pH: mathematical measure of acidity and alkalinity, expressed as negative logarithm:

1. Acidic substances have higher concentrations of hydrogen (H⁺) ions and therefore can give up more H⁺ ions; alkaline (base) substances have lower concentrations of H⁺ ions and can accept more H⁺ ions.

2. The pH of normal tissue is 7.4; pH of inflamed tissue is lower, between 5 and 6 (more acidic).

3. Decreased extracellular pH does NOT decrease nerve action; internal pH of a nerve is constant; decreased extracellular pH does decrease action of an anesthetic.

4. The pH of anesthetic without epinephrine (vasoconstrictor) is 5.5; anesthetic with epinephrine is ∼3.3 pH.

a. Manufacturers acidify anesthetic to inhibit oxidation (breakdown) of epinephrine.

b. Anesthetic may burn slightly on deposition because of difference between pH of anesthetic and pH of tissues.

c. MORE acidic the anesthetic, slower its onset; using cartridge warmers, can break down pH of local anesthetic, increasing the burning during deposition (also destroys the vasoconstrictor).

D. Dissociation of local anesthetics: ability of a local anesthetic to dissociate, indicated by pK_a number.

1. The pK_a number is a constant that characterizes equilibrium of a particular compound; also measures molecule’s affinity for H⁺ ions:

a. Equilibrium equation is the pK_a equation:

b. Cation: RNH⁺ is a positively charged molecule that is responsible for binding at the receptor site and decreasing the Na⁺ that enters the nerve.

c. Free base: RN is an uncharged molecule that is responsible for the diffusion of anesthetic through surrounding tissues and the nerve sheath.

2. Clinical implications of the pK_a number, since each anesthetic has pK_a number:

a. Lower the pK_a number (below 7.5), the MORE lipophilic free base molecules (creates greater diffusion, quicker onset, longer duration), but the LESS cations available to bind the anesthetic.

b. When the pH of anesthetic is same as the pK_a number, equal amounts of BOTH base and cation exist.

c. Equilibrium shifts:

(1) Shifts left (cation state) when there are MORE hydrogen ions (low pH).

(2) Shifts right (free base state) when there are FEWER hydrogen ions (high pH).

d. The MORE free base molecules available, the greater the diffusion of anesthetic through tissues and membrane, and therefore the faster the onset of action.

3. The pH of anesthetic is lowered with addition of epinephrine (pH 3.3):

a. When MORE cations exist, more Na⁺ is bound at the nerve receptor, which creates greater binding power.

b. LESS free base leads to less diffusion and slower onset.

c. Surrounding tissues buffer MORE acidic solutions.

4. The pH of inflamed tissues is low (5 to 6), so MORE cations exist; therefore MORE Na⁺ is bound at nerve receptor site:

a. LESS diffusion of anesthetic into surrounding tissues causes slower onset and leads to ineffective anesthesia.

b. Surrounding tissues are NOT able to buffer more acidic solutions because of lower pH.

c. Patient may need MORE local anesthetic agent because of acidic conditions; block may be MORE effective than infiltration, since agent is NOT near inflamed tissues.

Figure 14-2 Chemical formula for a local anesthetic.

Pharmacology of Local Anesthetics and Vasoconstrictors

Understanding the metabolism, action, dosage calculations, and specific functions of topical and local anesthetic agents and vasoconstrictors helps the clinician to request and use these agents more safely and efficiently. Clinician MUST prevent an overdose (OD) situation, which is an accidental or intentional use of a drug in an amount higher than is normally used.

• See Chapter 9, Pharmacology: local anesthetic and vasoconstrictor pharmacology.

A. Types of agents:

1. Ester agents: NO longer available as injectables, ONLY topicals (usually 20% benzocaine):

a. Biotransformed to paraaminobenzoic acid (PABA) in blood plasma by enzyme pseudocholinesterase.

b. Half-life (rate at which 50% of the anesthetic is eliminated from the blood) is 2 to 8 minutes.

c. Have lower potential for OD (toxicity).

d. MORE likely to cause allergic reaction (to PABA).

2. Amide agents: BOTH injectables and topicals (NOT as useful at 5%) available:

a. LESS likely to cause allergic reaction because methylparaben, which can cause allergic reactions, has been eliminated as preservative.

b. Biotransformed MAINLY in liver (MUST have healthy liver tissue).

c. Have greater potential for OD (alone, without vasoconstrictor) because higher blood levels occur until agent reaches liver for biotransformation.

d. Half-life is 50 to 120 minutes.

(1) EXCEPTION: Articaine’s half-life is different from other amides.

(a) Falls under amide class, but its associated ester group also allows plasma metabolism via pseudocholinesterase, purportedly increasing rate of breakdown and reducing its toxicity.

(b) Difference in metabolism gives advantage of having a 30-minute half-life, in contrast to lidocaine, which has a 90-minute half-life.

B. Distribution and elimination of agents:

1. After entering blood, agents permeate ALL body tissues.

2. Are vasodilators; thus vasoconstrictors are added in MOST cases to decrease vasodilation.

3. Esters and amide agents are BOTH eliminated mostly through the kidneys.

C. Phentolamine mesylate (Oraverse): injection via syringe, which accelerates return of normal soft tissue sensation (i.e., sensation of lip and tongue), as well as function following restorative and periodontal procedures, and helps prevent any self-inflicted oral trauma that may occur with a long-lasting injection of local anesthetic containing a vasoconstrictor; contains an alpha-adrenergic antagonist that acts as a vasodilator, resulting in faster diffusion of anesthetic into the cardiovascular system and away from site.

Local Anesthetic Agent Action

Local anesthetic is an anesthetic drug that induces local anesthesia by inhibiting nerve excitation or conduction. These agents also have effects on central nervous system (CNS), cardiovascular system (CVS), respiratory system.

• See Chapter 10, Medical and Dental Emergencies: local anesthesia emergency protocol in a dental setting.

A. CNS effects:

1. Low levels have NO effect but can provide anticonvulsive properties by raising seizure threshold; used to treat epileptic seizures.

2. Preconvulsive levels can cause slurred speech, shivering, twitching, flushed feeling, dream state, lightheadedness, blurred vision, tinnitus.

a. Lidocaine may cause mild sedation or drowsiness, indication of possible toxic reaction.

b. Therefore anesthetized patient should NEVER be left alone, since onset occurs in 5 to 10 minutes.

3. Convulsive levels cause convulsions, CNS depression, respiratory depression and arrest.

B. CVS effects:

1. Low levels produce NO effects.

2. High (non-OD) levels cause mild hypotension (low blood pressure) by relaxing smooth muscles.

3. At OD levels, can produce profound hypotension, which causes decreased myocardial contractions, decreased cardiac output, decreased peripheral resistance.

4. Lethal levels lead to CVS collapse caused by massive peripheral vasodilation, decreased heart contractions, and decreased heart rate (bradycardia).

C. Respiratory system effects:

1. Non-OD levels relax action of bronchial smooth muscles.

2. OD levels can lead to respiratory arrest as result of CNS depression.

Vasoconstrictor Action

Vasoconstrictors if used in local areas cause constriction of the arterioles and capillaries. Vasoconstrictors act on alpha (α) and/or beta (β) receptors, depending on the body tissues.

A. Chemical structure of a vasoconstrictor (Figure 14-3):

1. Benzene ring with two OH groups in the third and fourth positions is a catechol.

2. Benzene ring with an amine group in another position is a catecholamine.

3. MOST vasoconstrictors are catecholamines:

a. Epinephrine, norepinephrine, dopamine: ALL occur in nature.

b. Levonordefrin and isoproterenol: BOTH synthetics.

4. Do NOT use cartridge warmers, since inactivate vasoconstrictors.

C. Types of vasoconstrictors:

1. Epinephrine (adrenalin): one MOST commonly used in United States:

a. MORE potent; found in BOTH natural and synthetic forms.

b. In skeletal muscle and blood vessels, produces both vasodilation (small amounts act on β2 sites) and vasoconstriction (large amounts act on α receptors).

c. MAINLY used at 1:100,000 for nerve blocks and not 1:50,000 concentrations (usually only infiltrations and intraseptal injections); use of additional dosage does NOT increase duration and/or effectiveness, ONLY hemorrhage control.

2. Norepinephrine (Levarterenol): NOT used in United States, but used in other countries:

a. LESS potent than epinephrine (one fourth as potent) and demonstrates LESS systemic action.

b. Activation of α receptors in the smooth muscles of palatal blood vessels can cause ischemia and then tissue necrosis.

3. Levonordefrin (Neo-Cobefrin): NOT as commonly used in United States:

a. LESS potent than epinephrine (one fifth as potent); demonstrates LESS systemic action so used at higher concentration (1:20,000) when used with agents such as 2% mepivacaine; has same onset, depth, duration of anesthesia in both pulpal and soft tissue as lidocaine with epinephrine.

b. NOT as strong in hemorrhage control as epinephrine (IMPORTANT in dental procedures involving bleeding and need for hemorrhage control, such as dental hygiene procedures).

D. Inclusion of vasoconstrictors:

1. Medical considerations for use of vasoconstrictors:

a. Absolute contraindications:

(1) Cardiovascular disease (CVD): acute incident (myocardial infarction [MI, heart attack] or cerebrovascular accident [CVA, stroke]) within last 4 to 6 weeks or unable to meet 4 METs (metabolic equivalents); high blood pressure (HBP) ≥140/90 mm Hg; unstable or severe angina pectoris that is relieved by rest.

(2) With uncontrolled or undiagnosed hyperthyroidism, may cause thyroid storm.

(3) Recreational cocaine (crack) user (within 24 hours); could be fatal.

b. Relative contraindications:

(1) Reduced levels needed with MOST other chronic CVD histories; however, still may need to use a limited amount to ensure pain control (reduces endogenous [own] epinephrine of patient with CVD); see next section.

(2) Patients taking tricyclic antidepressants (TCAs): NEITHER norepinephrine NOR levonordefrin (Neo-Cobefrin) should be used; substitute epinephrine if needed.

2. Consideration for duration of appointment:

a. Addition increases duration of anesthetic effects.

b. Concentration and type affect duration of a local anesthetic.

3. Consideration for hemostasis during appointment:

a. Epinephrine in large quantities acts as a vasoconstrictor; in smaller quantities becomes vasodilator that has potential to increase bleeding postoperatively.

b. Injection SHOULD be close to the area of bleeding to be effective; may want to add epinephrine 1:50,000 levels (available with lidocaine agent) as interseptal injection after other injections.

c. Epinephrine has BETTER hemostatic control levels than levonordefrin (Neo-Cobefrin), which is important with bleeding that may occur with nonsurgical periodontal maintenance.

E. Vasoconstrictor use causes slight burning upon injection (MORE than with plain) because of presence of preservative (sodium metabisulfate), since it is acidic to increase agent’s shelf-life (discussed later) but this side effect does not preclude use or add need for plain preinjection.

Figure 14-3 Chemical structure of a vasoconstrictor.

Dosage Calculations

Dosage calculations for local anesthetics are based on the size and general health of patient and on type and concentration of the anesthetic agent and vasoconstrictor. The maximum recommended dose (MRD) is the dose established by manufacturer (in milligrams per pound).

A. MRD for each anesthetic agent (Box 14-1).

B. Concentration of vasoconstrictors: ratio of vasoconstrictor to milliliters of solution (Box 14-2).

1. MRD of epinephrine:

a. MRD for healthy patient is 0.2 mg per appointment.

b. MRD for patient with CVD is HALF as much: 0.04 mg per appointment.

2. MRD of levonordefrin (Neo-Cobefrin) for all patients is 1.0 mg per appointment.

Box 14-1 Local Anesthetic Agent Dose Calculations

EXAMPLE: LOCAL ANESTHETIC AGENT DOSE CALCULATION USING 2% LIDOCAINE FOR 150 LB PATIENT

1. Percentage grams to milligrams/milliliter: 2% ÷ 100 = .02 g/mL x 1000 mg/g = 20 mg/mL.

2. Milligrams per cartridge: 20 mg/mL x 1.8 mL/cartridge = 36 mg/cartridge.

3. Patient MRD: 2 mg/lb (MRD) x patient’s weight (e.g., 150 lb) = 300 mg.

4. Milliliters of solution: 300 mg ÷ 20 mg/mL = 15 mL.

5. Number of cartridges per patient: 15 mL ÷ 1.8 mL/cartridge = 8.3 cartridges.

Fast Tip: Eliminate steps 4 and 5 by dividing mg MRD/patient by 36 mg/cartridge: 300 mg ÷ 36 mg/cartridge = 8.3 cartridges.

MRD, Maximum recommended dosage by manufacturer.

Box 14-2 Calculation of Vasoconstrictor Concentration

1. To change grams to milligrams, multiply by 1000, since ratio equals 1 gram of drug per milliliters of solution.

2. To find mg of vasoconstrictor drug per mL of solution (mg/mL), divide mg of drug by mL of solution.

3. To find mL of solution, divide MRD∗ of vasoconstrictor in mg by mg/mL.

4. To find number of cartridges, divide MRD mL of solution by 1.8 mL/cartridges.

EXAMPLE: CALCULATION OF CONCENTRATION OF VASOCONSTRICTORS USING 1:100,000 EPINEPHRINE/ML OF SOLUTION

1. Ratio: 1:100,000 = 1 g of drug per 100,000 mL of solution.

2. 1 g = 1000 mg of drug per 100,000 mL of solution.

3. 1000 mg ÷ 100,000 mL = 0.01 mg/mL.

EXAMPLE: VASOCONSTRICTOR DOSE CALCULATION FOR HEALTHY ADULTS AND CVD PATIENTS USING EPINEPHRINE

MRD for healthy adult patient: 0.2 mg per 1:100,000 epinephrine.

MRD for patient with CVD: 0.04 mg per 1:100,000 epinephrine.

How many cartridges of anesthetic with epinephrine can a healthy adult have?

0.2 mg of drug ÷ 0.01 mg/mL = 20 mL; then 20 mL ÷ 1.8 mL/cartridge = 11.11 cartridges.

How many cartridges of anesthetic with epinephrine can a patient with CVD have?

0.04 mg of drug ÷ 0.01 mg/mL = 4 mL; then 4 mL ÷ 1.8 mL/cartridge = 2.2 cartridges.

Note: Levonordefrin [Neo-Cobefrin] allows 1 mg vasoconstrictor/any patient/visit.

MRD, Maximum recommended dosage by manufacturer; clinicians may be more conservative in use.

Local Anesthetic Agents and Vasoconstrictors

Vasoconstrictors and local anesthetic agents must be chosen carefully, based on the medical concerns and type of dental procedure to be performed. Anesthetic is selected based on whether its duration is appropriate to procedure being performed.

A. Selection considerations:

1. Medical concerns (if vasoconstrictor used, see earlier discussion):

a. True allergy to local anesthetic agent is rare (past history may be to esters, usually NOT to amides); may be allergic to preservative for vasoconstrictor (sodium metabisulfite); try plain anesthetic agent.

b. CVD concerns include incident (MI, CVA) within last 4 to 6 weeks or unable to meet 4 METs, HBP ≥140/90 mm Hg, unstable or severe angina pectoris, uncontrolled or undiagnosed hyperthyroidism.

c. Pregnant patients (use category B: lidocaine and prilocaine, NOT category C: mepivacaine, articaine, bupivacaine).

2. Onset and duration:

a. Onset is determined by properties of local anesthetic agent, including its dissociation.

b. Duration (short, medium, or long acting) is determined by site of injection, type of anesthetic agent, addition of vasoconstrictor, patient’s idiosyncrasies (Tables 14-1, 14-2, and 14-3).

B. Local anesthetic agents with and without vasoconstrictors (plain):

1. Lidocaine, mepivacaine, prilocaine are available BOTH with vasoconstrictor and without (plain).

2. Bupivacaine, articaine, etidocaine are available with vasoconstrictor.

Table 14-1 Short-acting local anesthetics

Table 14-2 Medium-acting local anesthetics

Table 14-3 Long-acting local anesthetics

Topical Anesthetics

Topical anesthetics are useful for providing light, localized anesthesia to the first 2 to 3 mm of the oral mucosa as a preinjection agent. May also be used alone before procedures involving soft tissues (nonsurgical periodontal therapy). Must be placed on oral mucosa for 2 to 3 minutes per Materials Safety Data Sheet (MSDS).

• See Chapter 9, Pharmacology: discussion of topical anesthesia using gel or patch.

B. Concern for allergenic potential (see earlier discussion).

Local Anesthesia Armamentarium

Preparing the armamentarium for delivery of local anesthetic involves knowledge of the syringe, needle, cartridge, proper setup procedures, care of equipment, safe handling, and prevention and management of associated problems. Aspiration is the process of removing fluids (or gases) from the body with a suction device (syringe with piston). It allows the clinician to know if the needle tip is in a blood vessel to prevent an intravascular injection.

1. Syringe types:

a. Harpoon syringe: MOST commonly used one (Figure 14-4):

b. Self-aspirating syringe (Figure 14-5):

(1) Metal projection presses on rubber diaphragm of the cartridge; pushing on the thumb ring increases the pressure of projection on the diaphragm.

(2) Thereby increases pressure inside the cartridge, aspiration occurs, then pressure is released.

c. High-pressure syringe (Ligmaject):

(1) Used MAINLY for periodontal ligament (PDL) (intraligamentous) injection (type of intraosseous injection), which permits measured dose of solution and overcomes tissue resistance; for other PDL injection with traditional syringe, see Table 14-4.

(2) May cause trauma to surrounding tissues if increased solution (under pressure) is forced into PDL space; if this situation occurs with primary teeth, can also cause trauma to developing permanent teeth.

d. Safety syringes (UltraSafe, Safety Plus): LESS risk of needlestick injury (see later discussion).

2. Handling of syringes: should be checked for rust, harpoon sharpness, working piston.

a. Leakage during injection: caused by offset needle placement into rubber diaphragm or by loose needle.

b. Broken cartridge: caused by too much pressure when engaging harpoon or by bent harpoon.

c. Disengagement of harpoon during aspiration: caused by dirty, dull, or broken harpoon or NOT securely engaging rubber stopper in cartridge.

B. Needles: stainless steel, disposable, presterilized, sharp to decrease potential for cross-contamination (Figure 14-6):

1. Bevel: oblique surface to penetrate soft tissue without resistance; placed toward bone to prevent trauma to overlying periosteum (bone’s surface).

2. Shank: length is measured from bevel tip to the hub:

a. Short shank: ∼1 inch/∼25 mm.

b. Long shank: ∼1.58 inches/∼40 mm.

3. Gauge: measure of inside diameter of lumen; larger the number, smaller the needle; thus smaller to larger: 30, 27, 25-gauge.

a. Smaller gauge needles (30-gauge) with smaller lumen are NOT recommended for less pain:

(1) Deflect MORE when penetrating tissues, reduces accuracy because solution is deposited away from intended site.

(2) Smaller lumen increases possibility of clogging needle with blood cells, MORE likely to show false-negative aspiration.

b. Larger gauge needles (27- to 25-gauge) with larger lumen are BEST, with long shank with 25 gauge and short shank with 27 gauge.

(1) Deflect LESS when penetrating tissues, increasing accuracy because solution is deposited close to intended site.

(2) Easier to aspirate, since increases true-negative aspiration, LESS likely to show false-negative aspiration.

(3) Short shank needles with 27-gauge are used on MOST commonly administered injections, EXCEPT inferior alveolar nerve block (and thus buccal nerve block done immediately after) uses long shank with 25-gauge.

4. Hub or needle adapter: some have bevel indicator dots.

5. Cartridge-penetrating end: sharp to penetrate rubber diaphragm of cartridge.

6. Needle cap/sheath.

C. Cartridges: cylindrical tube of agent, color-coded by manufacturer to distinguish types, holds 1.8 mL of anesthetic (Figure 14-7):

1. Rubber stopper: coated with silicone to ease movement, engaged by harpoon, then pushed by piston to dispel solution; may/may not have rubber latex.

2. Aluminum cap: holds rubber diaphragm in place.

3. Rubber diaphragm: acts as seal to prevent anesthetic from leaking around needle, as long as needle penetrates the diaphragm squarely and NOT on an angle, does NOT have rubber latex.

4. Contents besides agent and vasoconstrictor (additives):

a. Hydrochloride (HCl): added to agent to create acidic salt for BETTER water solubility; increases diffusion of agent to nerve; makes anesthetic injectable.

b. Sodium chloride: added to make solution MORE isotonic with soft tissues.

c. Sodium metabisulfite: antioxidant that is added to preserve vasoconstrictor (if present) by reacting with oxygen to produce sodium bisulfate (more acidic, slight increase in burning during injection [MORE than plain]); can act as allergen.

d. Distilled water: provides remaining volume.

5. Handling of cartridges:

a. SHOULD be checked before use for clear solution without large bubbles, normal stopper, noncorroded/rusty cap.

(1) Bubbles that are small (1 to 2 mm): acceptable; however, larger bubbles mean that solution was frozen, which causes chemical changes.

(2) Extruded stopper: caused by freezing cartridge or by storing in disinfectant.

(3) Corroded/rusty cap: caused by cartridge breakage in round tin container (10-cartridge blister packs decrease breakage) or by immersion in disinfectant (metal cap).

b. With vasoconstrictors, shelf-life is shorter at 18 months; without vasoconstrictors, shelf-life is longer at 24 months.

c. Burning during injection: normal response to pH of agent; however, those containing disinfectant or vasoconstrictors and overheating (by cartridge warmer) can cause increased burning during injection.

d. To maintain viable anesthetic: do NOT autoclave, soak in disinfectant, or keep in direct sunlight or in warmers; wipe ends with 70% alcohol solution if NOT used.

D. Computer-controlled local anesthesia delivery (CLAD) system (CompuDent/Wand, Comfort Control):

1. BOTH use traditional cartridges and either traditional needles or safety (Luer-Lok) needles; provides MORE controlled amounts of anesthetic solution delivered for ALL types of injection techniques.

2. Handpiece is held with a pen grasp and is lighter than traditional syringes; as needle penetrates, clinician steps on a pedal/uses finger-touch control to activate flow of anesthetic solution ahead of needle path.

3. Has auto-aspiration feature that can be used for any type of injection; amount deposited for MOST injections is 0.6 to 0.9 mL.

4. MUST be used to perform AMSA block injection (discussed later).

Figure 14-4 Harpoon aspirating syringe.

Figure 14-5 Self-aspirating syringe.

Table 14-4 Periodontal ligament injection technique ^∗

Anatomy anesthetized	Pulpal and soft tissue and nerve endings in area of injection
Needle gauge and length	27-gauge; short, extra short, or ultra short or CLAD
Depth of penetration	Base of pocket until resistance is met
Landmarks	Pocket area, mesial of distal root
Site of penetration	Long axis of root on mesial or distal with bevel toward root
Deposition site	Base of pocket
Cartridge amount (1.8 mL/cartridge)	0.2 mL
Complications	Pain
Advantages	Minimal dose required; no unnecessary structures anesthetized; works better with CLAD
Disadvantages	Leakage of anesthetic; difficult to deposit with nonpressure syringe; not with inflammation or primary teeth present

∗ See manufacturer’s directions for use of pressure syringe (Ligmaject); dental hygienists may not be allowed to perform intraosseous injections in some states.

Figure 14-6 Parts of a needle.

Figure 14-7 Components of an anesthetic cartridge.

CLINICAL STUDY

Scenario: During an initial dental hygiene appointment with new patient, the dental hygienist observes blood in a cartridge (positive aspiration) during administration of an inferior alveolar nerve (IA) nerve block (2% lidocaine with 1:100,000 epinephrine). A 25-gauge long needle is being used. A large amount of blood fills the cartridge quickly. The patient with generalized moderate chronic periodontitis reports no medical conditions and exhibits no significant need for dental restoration.

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Tags: Saunders Review of Dental Hygiene

Jan 1, 2015 | Posted by mrzezo in Dental Hygiene | Comments Off

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