Essentials in Dentistry (A Student’s Manual) Priyanka Jain, Balaram Naik
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ANALGESIA AND SEDATIONCHAPTER 1

Priyanka Jain
 
LOCAL ANESTHETICS
 
Introduction
Local anesthetics are chemical agents that produce loss of sensation to pain in a specific area of the body without the loss of consciousness by the depression or excitation in the nerve endings. In clinical dental practice, a localized loss of pain is desired. Although dental analgesia and dental anesthesia are used synonymously in dentistry, local analgesia is more accurate. Local anesthesia can be achieved by a number of different mechanisms including the use of neurolytic agents in addition to the traditional agents. However, in clinical dental practice, only reversible local anesthetic agents are used. These agents block the nerve conduction impulses reversibly and can be administered via a spray, drops or an injection. The most common route of administration is by injection to the area requiring numbing. This works as the anesthetic selectively targets nerves to block them transmitting pain signals and sending them to the brain.
The use of reversible local anesthetic chemical agents is the most preferred method of achieving pain control in dental practice. Some ideal properties of a local anesthetic agent are:
  • Reversible action
  • Nonirritant
  • Should not produce any secondary local reactions like allergies
  • Should have rapid onset
  • Potent in nature
  • Should have sufficient penetrating properties
  • Should be stable in its form
  • Should not interfere with the healing of local tissues
  • Nonaddictive
  • Suitable duration of action
  • No systemic toxicity
  • Sterilizable without the loss of properties.2
 
Classification
Local anesthetics can be classified according to their (Table 1.1):
 
Chemical Structure
  • Amides
  • Esters.
 
Duration of Action
  • Short acting
  • Intermediate acting
  • Long acting.
 
Mechanism of Action of Local Anesthetics
All local anesthetics agents used in dentistry work by obstructing the exchange in Na+ permeability which is essential for the initial phases of a neuronal action potential. In general terms, these agents prevent nerve conduction by obstructing the depolarization which is effected by the influx of sodium ions. In the axon wall there are numerous pores which allow the ionic changes (influx of sodium ions). Local anesthetics (LA) cations block these channels. As a result, the nerve loses the capacity to create the impulse and the patient loses the sensation in the area supplied by the nerve.
 
LOCAL ANESTHETIC SOLUTION
 
Constituents
  • Vasoconstrictor: This is added to delay the removal of the anesthetic by decreasing the blood flow. A vasoconstrictor has the following advantages—(a) longer duration of action of the local anesthetic agent (b) reduces bleeding at the injection site and (c) has reduced systemic effects.
    Table 1.1   Various types of local anesthetics used in dentistry
    Local anesthetic
    Type
    Duration of action
    Lidocaine
    Amide
    Intermediate
    Prilocaine
    Amide
    Intermediate
    Mepivacaine
    Amide
    Intermediate
    Bupivacaine
    Amide
    Long acting
    Etidocaine
    Amide
    Long acting
    Articaine
    Amide with an ester side chain
    Intermediate
    Procaine
    Ester
    Short acting
    3
    The most commonly used vasoconstrictors in dental anesthetic agents are epinephrine (adrenaline) and octapressin (felypressin). Certain chemicals are included in local anesthetic to protect the vasoconstrictor drug from being broken down. Contraindications of local anesthesia with vasoconstrictor include diabetics (as they increase the blood glucose level by counteracting the action of Insulin), hypertensive patients, cardiac patients (as they produce tachycardia and increased heart rate), pregnancy (as they can cause uterine contractions and may sometimes cause abortion), extraction of teeth with chronic peri apical sepsis (as they decrease the blood flow to the tissues which may lead to dry socket), and hyperthyroidism.
  • Reducing agent: This prevents the oxidation of the vasoconstrictor and acts by competing with the vasoconstrictor for the oxygen available in the solution. Sodium metabisulphite (0.5 mg/mL) is most commonly used.
  • Fungicide: Thymol is used as a fungicide. Sodium hydroxide is included to enhance the numbing effect of the drug.
  • Preservative: This helps to prolong the shelf life of the solution. They are bacteriostatic in nature. The typical shelf life of an anesthetic agent without preservative is approximately 18 months to 2 years. Methylparaben (1 mg/mL) is added as a preservative to articaine.
 
Structure
The injectable local anesthetics used in dentistry have a common core structure consisting of:
  • Hydrophilic amino terminal
  • Intermediate chain
  • Lipophilic aromatic terminal.
The combination of hydrophilic and lipophilic properties is essential in one molecule for the local anesthetic to be effective (Fig. 1.1). The hydrophilic portion of the anesthetic consists of a substituted secondary or tertiary amine. This hydrophilic property (solubility in water) is essential to allow for the dissolution in a solvent to permit injection and to allow sufficient penetration through the interstitial fluid after injection. The lipophilic part of the anesthetic molecule is an aromatic residue that is essential for its ability to penetrate fatty tissue such as lipid sheaths of nerves to reach its site of action.
The intermediate chain consists of either an amide or ester linkage. This allows the spatial separation of the hydrophilic and the lipophilic components of the molecule.4
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Fig. 1.1: Structure of a local anesthetic molecule
 
Differences of Esters and Amides
All local anesthetics are weak bases. Chemical structure of the local anesthetic molecule have an amine group on one end connected to an aromatic ring on the other and an amine group on the right side (Fig. 1.2). The amine end is hydrophilic (soluble in water) and the aromatic head is lipophilic (soluble in lipids). Therefore, a local anesthetic molecule can either have an amide group (Fig. 1.3) or an ester group (Fig. 1.4).
The older agents like procaine and cocaine were ester based but are no longer used due to their unwanted side effects of allergic reactions.
Different drugs have different proportions of hydrophilic and lipophilic components. These differences modify the characteristics and/or the properties of the anesthetic agents (Table 1.2).
 
Factors Affecting the Reaction of Local Anesthetics
Lipid Solubility: All local anesthetics are weak bases. Increasing the lipid solubility leads to faster nerve penetration and increases the onset of action. Onset of action is also dependent upon the proximity of the site of injection to the nerve to be anesthetized and the diameter of the nerve fibers. Thin fibers are anesthetized more rapidly as compared to thick fibers possibly because the nodes of Ranvier are closer together.
pH Influence: pH of the local anesthetics ranges from 7.6 to 8.9. Decrease in the pH shifts the equilibrium towards the ionized form of the local anesthetics thus delaying the onset of action.
Duration of Action: This is dependent on the rate of diffusion along a concentration gradient away from the site of injection. Lower vasodilator activity of a local anesthetic leads to slower absorption and longer duration of action (Table 1.3). Other factors affecting the duration and depth of the local anesthesia can be:
  • Patient factors: Children with problems of pediatric anesthesia, individuals with learning difficulties may be uncooperative and communication may be challenging, or patients who are highly anxious and needle phobic.5
    zoom view
    Fig. 1.2: Chemical structure of local anesthetics
    zoom view
    Fig. 1.3: Local anesthetic molecule with the amide link
    zoom view
    Fig. 1.4: Local anesthetic molecule with the ester link
    Table 1.2   Differences between amide and ester groups of local anesthetics
    Amide
    Ester
    • Amide link between intermediate chain and aromatic ring
    • Metabolized in the liver by amidase enzymes
    • Soluble in the solution
    • Ester link between intermediate chain and aromatic ring
    • Metabolized in the plasma through pseudocholinesterases and in the liver by lipase enzyme
    • Stable in the solution
    • Causes allergic reactions
    6
    Table 1.3   Some commonly used local anesthetics in dentistry
    Anesthetic
    Onset
    Duration (with epinephrine) in minutes
    Procaine
    Slow
    45-90
    Lidocaine
    Rapid
    120-240
    Bupivacaine
    Slow
    4-8 hours
    Table 1.4   Maximum recommended doses
    Drug
    Maximum dose
    Equivalent cartridges
    Lidocaine (lignocaine)
    4.4 mg/kg
    6-7 cartridges of 2.2 mL
    Prilocaine
    6 mg/kg
    For 3% prilocaine about 5-6 cartridges of 2.2 mL
    For 4% prilocaine about 4 cartridges of 2.2 mL
    Articaine
    7 mg/kg
    4 cartridges of 2.2 mL
    In such patients there may be high levels of autonomic activity with increased propensity to arrhythmias and vasovagal responses.
  • Factors related to the type of technique: Type of technique (infiltration or a nerve block), volume of solution and the accuracy of technique.
Effects on Other Tissues Including Toxicity: The functions of lipid containing organs and tissues such as the brain and heart may be affected by high levels of local anesthetics. Toxicity is the peak circulation levels of local anesthetics. Levels of local anesthetics administered to patients are varied according to age, weight and health. Some common toxic effects are light headedness, shivering or twitching, seizures, hypotension and numbness (Table 1.4).
Rate of Degradation: Amide local anesthetics are broken down by hepatic dealkylation and hydrolysis and excreted in the urine. Esters are metabolized by esterases.
 
Failure of Anesthesia
Failure to achieve profound analgesia during treatment procedure may be related to a variety of factors, like:
  • Inaccurate anatomic placement of the anesthetic solution
  • Injecting too little solution
  • Allowing insufficient time for the solution to diffuse and take effect7
  • Injecting into infected or inflamed tissues
  • Using an outdated or improperly stored anesthetic solution.
A local anesthetic should not be injected in inflamed tissues because of the risk of spreading the infection and the increased probability of achieving less than effective anesthesia due to the low pH within the infected tissue which maintains the ionized and the nonlipid soluble state of the anesthetic.
 
Complications of Local Anesthetics
These include both local and systemic effects.
 
Local Complications
Spread of Infection: Infection may spread into the tissues due to the needle passing through a contaminated tissue or the needle being contaminated before use.
Hematoma: Damage of a blood vessel by the tip of the needle may cause bleeding into the tissues. Small hematomas (in sulcus) are of little significance but significant bleeding may produce swelling and cause pain and trismus.
Needle Fracture: The chances are less likely due to the disposable use of needles these days.
Needle Stick Injury: The risk can be minimized by needle sheathing or the use of safe syringes.
Trismus: This occurs after inferior dental (ID) block and is attributed to damage in the medial pterygoid muscle. Either injection given too low or faster rate of deposition are the common factors. Management usually involves reassurance and encouragement to open the mouth slowly. If needed, antibiotics can be prescribed.
Blockage of the Facial Nerve: If the injection is given in close proximity to the facial nerve, a motor blockage causing temporary paralysis of the facial muscles may occur. The effect can last for 1–2 hours. In these cases, the desired branch of the trigeminal nerve will not be anesthetized.
Nerve Damage: Very rarely, the tip of the needle may pierce or hit a nerve bundle during injection causing an immediate electric shock like sensation to the patient. A complete return to normal sensation occurs soon.
 
Systemic Complications
Syncope: This is the most common systemic complication. It can be minimized by administering LA with patient in a supine position.8
Allergy: Some drugs may react with the anesthetic solution that causes allergies to the patient. For this, dentists should be careful keeping the medical history of the patient in mind.
Regional Infection: Infection can spread within the perioral tissues through planes of the head and neck by the passage of the needle through an infected area.
Cardiovascular Risk/Collapse: This may be related to stress in a susceptible patient (patients with angina pectoris, previous myocardial infarction or who have had previous cardiac surgery or circulatory dysfunction like cardiac failure. Excessive amounts of LA, faster delivery of the anesthetic solution and lack of aspiration can be contributing factors. The maximum safe dose of the lidocaine should be halved in such patients.
Liver Disease: Patients with reduced hepatic function may exhibit an increased rate of metabolism of the amide type of local anesthetics. Dosage levels should therefore be adjusted for these patients.
Methemoglobinemia: This is caused by a metabolite of prilocaine which reduces their oxygen delivering capacity and results in hypoxia. This is a rare complication.
 
DRUGS USED IN DENTAL ANESTHESIA
The drugs used for anesthesia in dentistry are (Table 1.5).
 
Lidocaine
In 1940, the first modern local anesthetic agent was lidocaine, trade name xylocaine. Used for blocks and infiltrations; however, effectiveness of analgesia is limited and of brief duration. This belongs to the amide class and causes little allergic reaction.
Table 1.5   Dilutions of the local anesthetic molecule
Dilution of local anesthetics
The dilution of an LA agent as 2% means that there is 2 grams (2000 mg) of LA agent in 100 mL of solution.
0.2% means 2 g/100 mL and 0.2% means 2000 mg/100 mL.
Dilution of vasoconstrictor
1:1000 means that there is 1 g (1000 mg) of vasoconstrictor in 1000 mL (1 L) of the solution or 1.0 mg/mL of the solution.
9
The addition of 1:80,000 epinephrine prolongs effectiveness to over 90 minutes.
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Prilocaine (Citanest)
This is less toxic in higher doses than lidocaine because of the small vasodilatory activity. Used for blocks and infiltrations, effective analgesia over 90 minutes, but predisposes to methemoglobinemia. It should be avoided in pregnancy.
 
Articaine (Septocaine)
This is the newest local anesthetic drug approved by the FDA in 2000. Its half-life is less than about one-fourth of lidocaine. This is used with a vasoconstrictor and enters the blood barrier smoothly. It is currently recommended for infiltration use only as it has rapid onset (<2 minutes) with exceptional ability to penetrate dense mandibular cortical bone. It is therefore ideal where blocks are contraindicated.
 
Bupivacaine (Marcaine)
This drug produces long anesthetic affect and is used for blocks and infiltrations where up to 8 h of anesthesia is required. This is available as 0.5% solution with a vasoconstrictor (Table 1.6).10
Table 1.6   Local anesthetic solutions
Duration
Solution
Infiltration (pulpal)
Nerve block (pulpal)
Soft tissue duration
Short duration - plain
• 2% lidocaine HCI
5 m
Not indicated
2 h
• Mepivacaine HCI 3%
20–30 m
45–65 m
2–3 h
• Prilocaine HCI 4%
10–15 m
45–65 m
3–4 h
Normal duration with vasoconstrictor
• Articaine HCI 4% with epi 1:100,000
60–75 m
Up to 120 m
3–5 h
• Articaine HCI 4% with epi 1:200,000
60–75 m
Up to 120 m
3–5 h
• Lidocaine HCI 2% with epi 1:50,000
55–65 m
80–90 m
3–5 h
• Lidocaine HCI 2% with epi 1:100,000
55–65 m
80–90 m
3–5 h
• Prilocaine HCI 4% with epi 1:200,000
35–45 m
50–70 m
3–6 h
Long duration
• Bupivacaine HCI 0.5% with epi 1:200,000
Up to 7 h
Up to 7 h
Up to 12 h
Abbreviations: epi, epinephrine; m, minutes; h, hours
 
DENTAL ANESTHETIC TECHNIQUES
There are various types of dental anesthetic techniques used. These are mentioned in brief below:
 
Infiltration
The anesthetic solution is deposited at/near the apex of the tooth and diffuses through the bone to affect the peripheral nerves and those nerves serving the periodontal ligament, adjacent bone and soft tissues. This may be used for minor procedures such as fillings.
 
Regional/Nerve Block
This is a common form of local dental anesthesia which blocks the reception of pain for one quadrant of the mouth at a time. This type of block is typically given in the buccal surface cheek. The anesthetic solution 11is deposited around a nerve trunk and causes anesthesia to tissues within the distribution of the nerve peripheral to the point of administration (Table 1.7). The different types of nerve blocks used in dentistry are:
  • Nasopalatine
  • Greater palatine
    Table 1.7   Types of nerve blocks
    Type of anesthesia
    Tissues anesthetized
    Comments
    Inferior dental nerve block
    • Mandibular teeth (including their pulp and periodontium), buccal gingivae from premolars to midline
    • Lower lip
    • Anterior two-thirds of the tongue
    • Floor of the mouth
    • Lingual gingivae
    The buccal gingivae and the sulcus in the molar region are not anesthetized fully and require separate infiltration of the long buccal nerve. The needle is introduced from premolars of the opposite side and inserted slightly above the occlusal plane lateral to the pterygomandibular raphae
    Mental nerve block
    • Mandibular first premolar to central incisor (including the pulp and the periodontium)
    • Lip, chin and adjacent sulcus and cheek of the above mentioned teeth
    Provides effective soft tissue analgesia. A lingual infiltration may be given for extractions
    Posterior superior alveolar
    • Upper molars
    Rarely indicated technique. The anesthetic solution is deposited distal to the maxillary second molar
    Infraorbital
    • Upper lip, cheek, side of the nose and lower eyelid
    • Buccal gingivae and sulcus from midline to premolar region
    • Incisors, canine and premolars
    The needle is aligned parallel to the long axis of the pre-molars while injecting
    Greater palatine
    • Palatal mucoperiosteum of the canine and posterior to it
    This injection is painful. Only a few drops need to be introduced very slowly for anesthesia. The anesthetic solution is deposited in the compressible area of the hard palate between the midline and the gingival margin of the teeth
    Nasopalatine
    • Palatal mucoperiosteum of the anterior hard palate related to canines and incisors
    This injection is also painful. A very small amount of anesthetic solution is required. Immediate blanching of the area is noted
    12
  • Inferior alveolar
  • Posterior superior
  • Mental nerve block
  • Infraorbital.
 
Intraosseous
An injection of local anesthetic is given directly into the osseous (bone) structure of the tooth. This provides profound single tooth analgesia.
 
Intraligamentary
The anesthetic solution is deposited along the periodontal membrane of individual teeth (to be anesthetized). This technique has the advantage of rapid onset and specific analgesia to isolated teeth and is a useful adjunct to conventional local anesthesia. The disadvantages include post injection discomfort due to temporary extrusion.
 
OTHER ANESTHETIC TECHNIQUES
 
Topical Anesthetics
Benzocaine (10–20%), eugenol, and forms of xylocaine (5–10%) are used topically to numb various areas before injections or other minor procedures. They produce their effect by acting on the free nerve endings (spray, gel or ointment). Ice bags can also be used for this purpose and act by means of refrigerant action on the surface of the mucous membrane. Another example is ethyl chloride.
 
General Anesthesia
Drugs such as midazolam, ketamine, propofol and fentanyl are used to put the patient in a twilight sleep or render them completely unconscious and unaware of pain.
 
Conscious Sedation
Conscious sedation is defined as a technique in which the use of a drug or drugs produces a state of depression of the central nervous system enabling treatment to be carried out, but during which verbal contact with the patient is maintained. The patient is able to retain their protective airway reflexes, and is able to respond to and understand verbal communication. It is a means to control an unmanageable child where all other means of restraint 13have failed. Patients should be carefully selected and medically pre-assessed and written consent must be obtained. The principal methods currently in use are inhalation, intravenous and oral although other methods are occasionally used.
 
Inhalation Sedation
A titrated mixture of up to 70% nitrous oxide may be administered. Clinical monitoring of patient color, respiration and pulse is required. It can be combined with an oral anxiolytic drug. Adult patients need not be accompanied home afterwards. This is the technique of choice in children felt to be candidates for sedation with mild and moderate anxiety and anxiety related gagging reflex. Works best in children aged 5 and above. Nitrous oxide (N2O), also known as “laughing gas”, easily crosses the alveoli of the lung and is dissolved into the passing blood, where it travels to the brain, leaving a dissociated and euphoric feeling for most patients. Nitrous oxide is used in combination with oxygen. Often (especially with children) a sweet-smelling fruity scent similar to an auto scent is used with the gas to inspire deep inhalation. The most common delivery system for this is the Quantiflex system. Written and informed consent is required for inhalational sedation. Advantages of conscious sedation include safe to use with minimal side effects, extremely useful in fearful, uncontrollable patients and provide comfortable and efficient dental treatment without compromising on quality.
Contraindications to Inhalational Sedation Include: These could be local or systemic. This technique cannot be used in patients with nasal obstruction, intolerance to mask, cold. Systemic contraindications include severe respiratory disease or mental/physical handicap.
 
Intravenous Sedation
Various intravenous sedatives have been used in the past. Titrated benzodiazepine is used to achieve anesthesia. Pulse oximetry and blood pressure monitoring is a must. Facilities must be available to administer oxygen or ventilation if needed.
It is relatively simple in comparison to general anesthesia. The technique is fast with few adverse effects and patient remains conscious throughout the procedure. Patients must be recovered appropriately and be accompanied by a responsible adult. Other intravenous agents used include a mixture of pentobarbitone, pethidine, hyoscine, and methohexitone. Advantages of intravenous sedation include sedation without loss of consciousness, verbal contact maintained with the patient during the procedure, and anterograde amnesia of 20–30 minutes duration.14
 
USE OF LOCAL ANESTHETICS
 
During Pregnancy
Any adverse drug interactions during pregnancy may affect either the mother or the fetus. Doses of dental local anesthetics are relatively small and are unlikely to cause any complications during pregnancy. All local anesthetics cross the placenta to some degree. Prilocaine has been found in highest concentration in the fetal circulation following its injection with bupivacaine as the lowest and lidocaine in between. Felypressin can cause uterine contractions; therefore it is best avoided in pregnancy although the dosage used in dental local anesthetics is very low to cause any unlikely effects. Lidocaine with epinephrine is most commonly used for pregnant patients. The anesthetics should have minimum epinephrine concentrations. Acetaminophen is the best analgesic used in pregnancy for dental patients. Penicillin, cephalosporin and erythromycin are the antibiotics of choice if needed. In the first trimester of pregnancy, radiographs should be limited to a minimum and performed only if deemed absolutely necessary.
 
In Children
Maximum recommended doses of local anesthetics are based on the weight of the child (expressed as mg/kg of the body weight). For obese children, maximum doses are calculated on the basis of ideal body weight and not the true body weight.
 
CONCLUSION
The level of anesthesia can be controlled to regulate how long the pain block lasts for as well as the level of numbness. This is meticulously controlled by concentration, amount administered as well as the actual solutions used in the anesthetic.
BIBLIOGRAPHY
  1. Aitkenhead Ar, Rowbotham DJ, Smith G. Textbook of Anesthesia, 4th edn. Churchill Livingstone,  Edinburgh,  2001.
  1. Cantlay K, Wiilaimson S, Hawkings J. Anesthesia for Dentistry. Continuing Education in Anesthesia, Critical Care and Pain. 2005; 5: 3.
  1. Meechan JG, Robb ND, Seymour RA. Pain and Anxiety Control for the Conscious Dental patient. Oxford University Press,  Oxford,  1998.
  1. Poswillo D. General anesthesia, sedation and resuscitation in dentistry. Report of an Expert Working Party for the Standing Dental Advisory Committee. Department of Health,  London:  1990.
  1. Robinson PD, Pitt Ford TR, Mc Donald F. Local anesthesia in dentistry. Wright,  Oxford,  2000.
  1. The Royal College of Anesthetists. Standards and Guidelines for General Anesthesia for Dentistry. The Royal College of Anesthetists,  London:  1999.