EXTRAORAL

EXTRAORAL  MANDIBULAR ANESTHESIA: INDICATIONS, COMPLICATIONS AND ITS TREATMENT. REMOVING THE TEETH OF THE MANDIBLE. INTRAORAL MANDIBULAR ANESTHESIA: INDICATIONS, COMPLICATIONS AND THEIR TREATMENT. REMOVING THE TEETH OF THE MANDIBLE.

 

Local or regional anesthesia involves the injection or application of an anesthetic drug to a specific area of the body, as opposed to the entire body and brain as occurs during general anesthesia. Purpose Local anesthetics are used to prevent patients from feeling pain during medical, surgical, or dental procedures. Over-the-counter local anesthetics are also available to provide temporary relief from pain, irritation, and itching caused by various conditions, such as cold sores, canker sores, sore throats, sunburn, insect bites, poison ivy, and minor cuts and scratches. Types of surgery or medical procedures that regularly make use of local or regional anesthesia include the following: biopsies in which skin or tissue samples are taken for diagnostic procedures childbirth surgeries on the arms, hands, legs, or feet eye surgery surgeries involving the urinary tract or sexual organs Surgeries involving the chest and abdomen are usually performed under general anesthesia. Local and regional anesthesia have advantages over general anesthesia in that patients can avoid some unpleasant side effects, can receive longer lasting pain relief, have reduced blood loss, and maintain a sense of psychological comfort by not losing consciousness. Description Regional anesthesia typically affects a larger area than local anesthesia, for example, everything below the waist. As a result, regional anesthesia may be used for more involved or complicated surgical or medical procedures. Regional anesthetics are injected. Local anesthesia involves the injection into the skin or muscle or application to the skin of an anesthetic directly where pain will occur. Local anesthesia can be divided into four groups: injectable, topical, dental (noninjectable), and ophthalmic.  Local and regional anesthesia work by altering the flow of sodium molecules into nerve cells or neurons through the cell membrane. Exactly how the anesthetic does this is not understood, since the drug apparently does not bind to any receptor on the cell surface and does not seem to affect the release of chemicals that transmit nerve impulses (neurotransmitters) from the nerve cells. It is known, however, that when the sodium molecules do not get into the neurons, nerve impulses are not generated and pain impulses are not transmitted to the brain. The duration of action of an anesthetic depends on the type and amount of anesthetic administered. Regional anesthesia Types of regional anesthesia include: Spinal anesthesia. Spinal anesthesia involves the injection of a small amount of local anesthetic directly into the cerebrospinal fluid surrounding the spinal cord (the subarachnoid space). Blood pressure drops are common but are easily treated. Epidural anesthesia. Epidural anesthesia involves the injection of a large volume of local anesthetic directly into the space surrounding the spinal fluid sac (the epidural space), not into the spinal fluid. Pain relief occurs more slowly but is less likely to produce blood pressure drops. Also, the block can be maintained for long periods, even days. Nerve blocks. Nerve blocks involve the injection of an anesthetic into the area around a nerve that supplies a particular region of the body, preventing the nerve from carrying nerve impulses to the brain. Anesthetics may be administered with another drug, such as epinephrine (adrenaline), which decreases bleeding, and sodium bicarbonate to decrease the acidity of a drug so that it will work faster. In addition, drugs may be administered to help a patient remain calm and more comfortable or to make them sleepy. Key terms Canker sore — A painful sore inside the mouth. Cold sore — A small blister on the lips or face, caused by a virus. Also called a fever blister. Epidural space — The space surrounding the spinal fluid sac. Malignant hyperthermia — A type of reaction (probably with a genetic basis) that can occur during general anesthesia in which the patient experiences a high fever, the muscles become rigid, and the heart rate and blood pressure fluctuate. Subarachnoid space — The space surrounding the spinal cord that is filled with cerebrospinal fluid. Topical — Not ingested; applied to the outside of the body, for example to the skin, eye, or mouth. Local anesthesia INJECTABLE LOCAL ANESTHETICS. These medicines are given by injection to numb and provide pain relief to some part of the body during surgery, dental procedures, or other medical procedures. They are given only by a trained health care professional and only in a doctor’s office or a hospital. Some commonly used injectable local anesthetics are procaine (Novocain), lidocaine (Dalcaine, Dilocaine, L-Caine, Nervocaine, Xylocaine, and other brands), and tetracaine (Pontocaine).

TOPICAL ANESTHETICS. Topical anesthetics, such as benzocaine, lidocaine, dibucaine, pramoxine, butamben, and tetracaine, relieve pain and itching by deadening the nerve endings in the skin. They are ingredients in a variety of nonprescription products that are applied to the skin to relieve the discomfort of sunburn, insect bites or stings, poison ivy, and minor cuts, scratches, and burns. These products are sold as creams, ointments, sprays, lotions, and gels. DENTAL ANESTHETICS (NON-INJECTABLE). Some local anesthetics are intended for pain relief in the mouth or throat. They may be used to relieve throat pain, teething pain, painful canker sores, toothaches, or discomfort from dentures, braces, or bridgework. Some dental anesthetics are available only with a doctor’s prescription. Others may be purchased without a prescription, including products such as Num-Zit, Orajel, Chloraseptic lozenges, and Xylocaine.

 OPHTHALMIC ANESTHETICS. Other local anesthetics are designed for use in the eye. The ophthalmic anesthetics proparacaine and tetracaine are used to numb the eye before certain eye examinations. Eye doctors may also use these medicines before measuring eye pressure or removing stitches or foreign objects from the eye. These drugs are to be given only by a trained health care professional. Recommended dosage The recommended dosage depends on the type of local anesthetic and the purpose for which it is being used. When using a nonprescription local anesthetic, follow the directions on the package. Questions concerning how to use a product should be referred to a medical doctor, dentist, or pharmacist. Precautions People who strongly feel that they cannot psychologically cope with being awake and alert during certain procedures may not be good candidates for local or regional anesthesia. Other medications may be given in conjunction with the anesthetic, however, to relieve anxiety and help the patient relax. Local anesthetics should be used only for the conditions for which they are intended. For example, a topical anesthetic meant to relieve sunburn pain should not be used on cold sores. Anyone who has had an unusual reaction to any local anesthetic in the past should check with a doctor before using any type of local anesthetic again. The doctor should also be told about any allergies to foods, dyes, preservatives, or other substances. Older people may be more sensitive to the effects of local anesthetics, especially lidocaine. This increased sensitivity may increase the risk of side effects. Older people who use nonprescription local anesthetics should be especially careful not to use more than the recommended amount.

Children also may be especially sensitive to the effects of some local anesthetics, which may increase the chance of side effects. Anyone using these medicines on a child should be careful not to use more than the amount that is recommended for children. Certain types of local anesthetics should not be used at all young children. Follow package directions carefully and check with a doctor of pharmacist if there are any questions. Regional anesthetics Serious, possibly life-threatening, side effects may occur when anesthetics are given to people who use street drugs. Anyone who uses cocaine, marijuana, amphetamines, barbiturates, phencyclidine (PCP, or angel dust), heroin, or other street drugs should make sure their doctor or dentist knows what they have used. Patients who have had a particular kind of reaction called malignant hyperthermia (or who have one or more family members who have had this problem) during or just after receiving a general anesthetic should inform their doctors before receiving any kind of anesthetic. Signs of malignant hyperthermia include fast and irregular heartbeat, very high fever, breathing problems, and muscle spasms or tightness. Although problems are rare, some unwanted side effects may occur when regional anesthetics are used during labor and delivery. These anesthetics can prolong labor and increase the risk of Cesarean section. Pregnant women should discuss with their doctors the risks and benefits of being given these drugs. Patients should not drive or operate other machinery immediately following a procedure involving regional anesthesia, due to numbness and weakness, or if local anesthesia also included drugs to make the patient sleep or strong pain medications. Injection sites should be kept clean, dry, and uncovered to prevent infection. Injectable local anesthetics Until the anesthetic wears off, patients should be careful not to injure the numbed area. If the anesthetic was used in the mouth, do not eat or chew gum until feeling returns. Topical anesthetics Unless advised by a doctor, topical anesthetics should not be used on or near any part of the body with large sores, broken or scraped skin, severe injury, or infection. They should also not be used on large areas of skin. Some topical anesthetics contain alcohol and should not be used near an open flame, or while smoking. Anyone using a topical anesthetic should be careful not to get this medication in the eyes, nose, or mouth. When using a spray form of this medication, do not spray it directly on the face, but apply it to the face with a cotton swab or sterile gauze pad. After using a topical anesthetic on a child, make sure the child does not get the medicine in his or her mouth. Topical anesthetics are intended for the temporary relief of pain and itching. They should not be used for more than a few days at a time. Check with a doctor if: the discomfort continues for more than seven days the problem gets worse the treated area becomes infected new signs of irritation, such as skin rash, burning, stinging, or swelling appear Dental anesthetics (non-injectable) Dental anesthetics should not be used if certain kinds of infections are present. Check package directions or check with a dentist or medical doctor if uncertain. Dental anesthetics should be used only for temporary pain relief. If problems such as toothache, mouth sores, or pain from dentures or braces continue, check with a dentist. Check with a doctor if sore throat pain is severe, lasts more than two days, or is accompanied by other symptoms such as fever, headache, skin rash, swelling, nausea, or vomiting. Patients should not eat or chew gum while the mouth is numb from a dental anesthetic. There is a risk of accidently biting the tongue or the inside of the mouth. Also nothing should be eaten or drunk for one hour after applying a dental anesthetic to the back of the mouth or throat, since the medicine may interfere with swallowing and may cause choking. If normal feeling does not return to the mouth within a few hours after receiving a dental anesthetic or if it is difficult to open the mouth, check with a dentist. Ophthalmic anesthetics When anesthetics are used in the eye, it is important not to rub or wipe the eye until the effect of the anesthetic has worn off and feeling has returned. Rubbing the eye while it is numb could cause injury. Side effects Side effects of regional or local anesthetics vary depending on the type of anesthetic used and the way it is administered. Anyone who has unusual symptoms following the use of an anesthetic should get in touch with his or her doctor immediately. There is a small risk of developing a severe headache called a spinal headache following a spinal or epidural block. This headache is severe when the patient is upright and hardly felt when the patient lies down. Though rare, it can occur and can be treated by performing a blood patch, in which a small amount of the patient’s own blood is injected into the area in the back where the anesthetic was injected. The blood clots and closes up any area that may have been leaking spinal fluid. Relief is almost immediate. Finally, blood clots or abscess can form in the back, but these are also readily treatable and so pose little risk. A physician should be notified immediately if any of these symptoms occur: large swellings that look like hives on the skin, in the mouth, or in the throat severe headache blurred or double vision dizziness or lightheadedness drowsiness confusion anxiety, excitement, nervousness, or restlessness convulsions (seizures) feeling hot, cold, or numb ringing or buzzing in the ears shivering or trembling sweating pale skin slow or irregular heartbeat breathing problems nusual weakness or tiredness  Local anesthetics provide a reversible regional loss of sensation. Local anesthetics reduce pain, thereby facilitating surgical procedures. Delivery techniques broaden the clinical applicability of local anesthetics.

These techniques include topical anesthesia, infiltrative anesthesia, ring blocks, and peripheral nerve blocks (see the Technique section below for links to detailed, illustrated articles demonstrating these techniques).  Local anesthetics are safer than general or systemic anesthetics; therefore, they are used whenever possible. In addition, they are relatively easy to administer and readily available. Local anesthetics have been undergoing development for centuries, and, as this article illustrates, research continues to provide surgeons with pharmacologic variety and to provide patients with anesthetic agents that have superior safety and efficacy profiles. Background Although the medical world cannot cure every disease, the control of pain to ensure patient comfort should be a goal. In 1860, cocaine, the oldest anesthetic, was extracted from the leaves of the Erythroxylon coca bush. In 1884, Sigmund Freud and Karl Koller were the first to use it as an anesthetic agent during ophthalmologic procedures.  Procaine, a synthetic alternative to cocaine, was not developed until 1904. Procaine is an ester of para-aminobenzoic acid (PABA). As procaine is metabolized, PABA, a known allergen, is released as a metabolic product.

The potential for severe allergic reactions limits the use of procaine and other ester-type anesthetic agents. Tetracaine, another ester-type anesthetic, was introduced in 1930. Tetracaine is more potent than procaine, and it causes similar allergic reactions.  In 1943, an alternative class of anesthetics was discovered when Lofgren developed lidocaine. This agent is an amide derivative of diethylaminoacetic acid, not PABA; therefore, it has the benefit of a low allergic potential. Since then, multiple amide-type anesthetics have been introduced into clinical use. Slight chemical alterations to the compounds have imparted beneficial characteristics, including increased duration and potency, to each. These compounds offer the surgeon more choices, and anesthetics can be appropriately matched to different procedures.  Pathophysiology Reviewing the physiology of nerve conduction is important before any discussion of local anesthetics. Nerves transmit sensation as a result of the propagation of electrical impulses; this propagation is accomplished by alternating the ion gradient across the nerve cell wall, or axolemma.  In the normal resting state, the nerve has a negative membrane potential of -70 mV. This resting potential is determined by the concentration gradients of 2 major ions, Na+ and K+, and the relative membrane permeability to these ions (also known as leak currents). The concentration gradients are maintained by the sodium/potassium ATP pump (in an energy-dependent process) that transports sodium ions out of the cell and potassium ions into the cell. This active transport creates a concentration gradient that favors the extracellular diffusion of potassium ions. In addition, because the nerve membrane is permeable to potassium ions and impermeable to sodium ions, 95% of the ionic leak in excitable cells is caused by K+ ions in the form of an outward flux, accounting for the negative resting potential.

The recently identified 2-pore domain potassium (K2P) channels are believed to be responsible for leak K+ currents.  When a nerve is stimulated, depolarization of the nerve occurs, and impulse propagation progresses. Initially, sodium ions gradually enter the cell through the nerve cell membrane. The entry of sodium ions causes the transmembrane electric potential to increase from the resting potential. Once the potential reaches a threshold level of approximately -55 mV, a rapid influx of sodium ions ensues. Sodium channels in the membrane become activated, and sodium ion permeability increases; the nerve membrane is depolarized to a level of +35 mV or more.  Once membrane depolarization is complete, the membrane becomes impermeable to sodium ions again, and the conductance of potassium ions into the cell increases.

The process restores the excess of intracellular potassium and extracellular sodium and reinstates the negative resting membrane potential. Alterations in the nerve cell membrane potential are termed the action potential. Leak currents are present through all the phases of the action potential, including setting of the resting membrane potential and repolarization.  Mechanism of action Local anesthetics inhibit depolarization of the nerve membrane by interfering with both Na+ and K+ currents. The action potential is not propagated because the threshold level is never attained. Although the exact mechanism by which local anesthetics retard the influx of sodium ions into the cell is unknown, 2 theories have been proposed. The membrane expansion theory postulates that the local anesthetic is absorbed into the cell membrane, expanding the membrane and leading to narrowing of the sodium channels.

This hypothesis has largely given way to the specific receptor theory. This theory proposes that the local anesthetic diffuses across the cell membrane and binds to a specific receptor at the opening of the voltage-gated sodium channel. The local anesthetic affinity to the voltage-gated Na+ channel increases markedly with the excitation rate of the neuron. This binding leads to alterations in the structure or function of the channel and inhibits sodium ion movement. Blockade of leak K+ currents by local anesthetics is now also believed to contribute to conduction block by reducing the ability of the channels to set the membrane potential.  On the basis of their diameter, nerve fibers are categorized into 3 types. Type A fibers are the largest and are responsible for conducting pressure and motor sensations. Type B fibers are myelinated and moderate in size. Type C fibers, which transmit pain and temperature sensations, are small and unmyelinated. As a result, anesthetics block type C fibers more easily than they do type A fibers. Therefore, patients who have blocked pain sensation still feel pressure and have mobility because of the unblocked type A fibers.  All local anesthetics have a similar chemical structure, which consists of 3 components: an aromatic portion, an intermediate chain, and an amine group (see molecular diagram below). The aromatic portion, usually composed of a benzene ring, is lipophilic, whereas the amine portion of the anesthetic is responsible for its hydrophilic properties.

The degree of lipid solubility of each anesthetic is an important property because its lipid solubility enables its diffusion through the highly lipophilic nerve membrane. The extent of an anesthetic’s lipophilicity is directly related to its potency.  Molecular diagram.  Local anesthetics are weak bases that require the addition of hydrochloride salt to be water soluble and therefore injectable. Salt equilibrates between an ionized form and a nonionized form in aqueous solution. Equilibration is crucial because, although the ionized form is injectable, the nonionized base has the lipophilic properties responsible for its diffusion into the nerve cell membrane. The duration of action of an anesthetic or the period during which it remains effective is determined by its protein-binding activity, because the anesthetic receptors along the nerve cell membrane are proteins.  The intermediate chain, which connects the aromatic and amine portions, is composed of either an ester or an amide linkage (see molecular diagram above). This intermediate chain can be used in classifying local anesthetics. 

 Local Anesthetics Injections  Mandibular Blocks  The Inferior Alveolar Nerve Block        

Advantages Practitioner acceptance Faster onset than higher blocks Bony landmark Disadvantages Area of injection is vascular; 10 -15% chance of positive aspiration Unlikely to anaesthetize accessory nerves Unlikely to anaesthetize long buccal nerve Difficult to see landmarks in some patients (e.g., macroglossia) The landmarks for this injection are as follows: the coronoid notch (the greatest depression on the anterior border of the ramus), also called the external oblique ridge the internal oblique ridge the pterygomandibular raphe the pterygotemporal depression the contralateral mandibular bicuspids Technique Palpate the anterior ramus border at the coronoid notch Slide the finger or thumb posteriorly and medially until a ridge of bone is palpated. This is the internal oblique ridge. Insert the needle into soft tissue in the pterygotemporal depression, which is halfway between the palpating finger or thumb and the pterygomandibular raphe. Approximate the height of the injection by the middle of the palpating fingernail or thumbnail. Ensure that the barrel of the syringe is located over the contralateral mandibular bicuspids    CONT’D ▼  Insert until bone is contacted, and then withdraw ~1 mm. The depth of insertion for the average-sized adult is approximately 25 mm. Aspirate. Inject a full cartridge Onset and duration Onset for hard tissue anaesthesia is 3 to 4 minutes. Duration for hard tissue anaesthesia is 40 minutes to 4 hours, depending on the type of local anaesthetic used and whether a vasoconstrictor is used. It is unlikely that the long buccal nerve will be anaesthetized.  

Inferior Alveolar Nerve Block Gow-Gates Mandibular Block  Advantages Perceptible end point (bone) Fewer blood vessels at this level, therefore less chance of positive aspiration Long buccal nerve anaesthesia likely Possible longer duration of anaesthesia Less chance of anaesthetizing accessory nerves    Disadvantages Mouth wide open Must use extraoral landmarks, which may increase the difficulty of this procedure The landmarks for this injection are as follows: 10 mm above the coronoid notch the internal oblique ridge the pterygomandibular raphe the neck of the condyle the contralateral mandibular bicuspids an imaginary line from the corner of the mouth to the tragal notch of the ear (extraorally). Technique Ask the patient to open his or her mouth wide. Palpate the coronoid notch and slide the finger or thumb to rest on the internal oblique ridge. Move the finger or thumb superiorly approximately 10 mm. Rotate the finger or thumb to parallel an imaginary line from the ipsilateral corner of the mouth to the tragal notch of the ear. Insert the needle at a point between the palpating fingernail and the pterygomandibular raphe at the middle aspect of the fingernail. Ensure that the barrel of the syringe is located over the contralateral bicuspids. As the injection proceeds, ensure that the angle of the needle and syringe is parallel to the imaginary line from the corner of the mouth to the tragus of the ear.    CONT’D▼ Insert until bone is contacted (at the neck of the condyle), which should occur at a depth of approximately 25 mm. (Note: This is not a deeper injection, because the patient’s mouth is open wide and, as a result, the condyle has translocated anteriorly to provide a target.) Once bone is  contacted, withdraw the needle tip 1 mm to prevent injecting into the periosteum, which would be painful. Aspirate. Inject a full cartridge.

Onset and duration Onset for hard tissue anaesthesia is 4 to 12 minutes, with the anterior areas taking the longest amount of time. The long buccal nerve will likely be anesthetised.   CONT’D

 

Gow-Gates Mandibular Block  Vazirani-Akinosi Closed Mouth Mandibular Block  Advantages Can be used for patients with trismus Can be used for patients with a strong gag reflex Mouth is closed, so injection may be less threatening to patient Possibly less pain, because tissues are relaxed Good for macroglossic patients   Disadvantages  Difficult to visualize depth of injection Difficult in patients with widely flaring ramus Difficult in patients with pronounced zygomatic ridge or internal oblique ridge  The landmarks for this injection are as follows: Difficult to visualize depth of injection Difficult in patients with widely flaring ramus Difficult in patients with pronounced zygomatic ridge or internal oblique ridge Technique Prepare the needle and syringe by bending the needle approximately 15^o to 20^o. This bend accommodates for the flare of the ramus. Do not bend the needle more than once when preparing. Ask the patient to slightly open (a few millimeters) his or her mouth and execute a lateral excursion toward the side that is being injected.  Palpate the coronoid notch and slide the finger or thumb to rest on the internal oblique ridge. Move the finger or thumb superiorly approximately 10 mm. Insert the needle tip between the finger and maxilla at the height of the maxillary buccal mucogingival line. Orient the bend of the needle such that the needle looks as though it is going laterally in the direction of the ear lobe on the injection side. The needle remains parallel to the occlusal plane.  After the needle has been inserted 5 mm, remove the palpating finger or thumb and use it to reflect the maxillary lip to enhance vision.

CONT’D▼ Inject to the final depth of approximately 28 mm for the average-sized adult, therefore visualizing 7 mm of needle remaining outside the tissue (if using a long needle). AspirateInject a full cartridge. Onset and duration Onset for hard tissue anaesthesia is 3 to 4 minutes There is an increased possibility of obtaining long buccal nerve anaesthesia as compared to the inferior alveolar nerve block.

Vazirani-Akinosi Closed Mouth Mandibular Block     Periodontal Ligament Injections  Advantages Immediate onset of anaesthesia No soft tissue anaesthesia Works well for “hot” teeth Good approach for accessory innervation High success rate  Disadvantages Patient may experience post-operative pain There is a transient decrease in pulpal blood flow to the tooth Cannot be used in areas of periodontal disease Pressure is required to inject into the PDL space Multiple injections are required for multi-rooted teeth (one injection per root) May not work on long roots (e.g., cuspids) Produces a Bacteremia (Roberts, 1997) Technique  Anaesthetize the soft tissue to allow for a comfortable PDL injection. Inject an infiltration of 0.2 mL to 0.3 mL of local anaesthetic into the buccal fold adjacent to the desired tooth.  Embed the needle into the PDL space Inject 0.2 mL per root. Allow 10 seconds to pass to allow back pressure to dissipate and ensure that local anaesthetic does not leak into the mouth upon removal of the needle.

Onset and duration The onset of anaesthesia is immediate. The duration of pulpal anaesthesia is highly variable and somewhat unpredictable.     .    CONT’D▼    Literature Support – How does PDL work? Meechan, 2002 – Supplementary routes to local aneaestheia.  Intraligamentary anaesthesia or periodontal ligament anaesthesia are, in a sense, misnomers. Solution injected via the periodontal ligament reaches the pulpal nerve supply by entering the cancellous bone through natural perforations in the socket wall, not by travelling down the length of the ligament Thus, this method is a form of intraosseous anaesthesia. Kim S, 1986 – Ligamental injection: a  physiological expaniation of efficacy   Intraligamentary anaesthesia is not a single tooth anaesthetic)  Kaufman et al, 1984  – Intraligamentary anesthesia: a double blind study.  The duration of intraligamentary anaesthesia is variable. 10 -15 minutes Gray et al. 1987

The presence of a vasoconstrictor significantly increases efficacy. reported that lidocaine with adrenaline was  effective in 91.6% of periodontal ligament injections whereas without the vasoconstrictor the success rate was only 42% Intraosseous – I don’t use this, higher medical risks  With intraosseous injections, the local anaesthetic solution is deposited directly into the cancellous bone surrounding the teeth being treated. Early techniques for delivering the local anaesthetic into the cancellous bone used a round bur to perforate the cortical plate, with the drug then being injected through this hole.  Advantages Immediate onset of anaesthesia No soft tissue (lip or tongue) anaesthesia Can operate bilaterally in the mandible Can anaesthetize a “hot” tooth Good approach for accessory innervation High success rate Disadvantages Short duration of anaesthesia     Must limit volume due to increased vascularity in the cancellous bone.  CONT’D▼ Difficult access to posterior mandible Anatomical limitations

Some patients experience palpitations Cannot use in areas of periodontal disease Technique Follow the specific instructions supplied with the delivery system. Anaesthetize the soft tissue to ensure that the perforation of the cortical plate is painless. Inject an infiltration of 0.2 mL to 0.3 mL of local anaesthetic into the buccal fold near the area to be perforated. Take a radiograph to ensure that there is enough bone at the perforation site so that the periodontal ligament space or root surfaces will not be violated. Perforate the bone using whichever device has been chosen. The site of perforation is on the attached gingiva approximately 1 mm to 2 mm coronally to the mucogingival line. Negotiate the needle through the perforated bone into the cancellous space and slowly inject 0.9 mL of local anaesthetic.  

This volume provides pulpal anaesthesia for the teeth on either side of the perforation. The injection should be done slowly, over about 45 seconds per 0.9 mL, to avoid palpitations as much as possible.  Do not exceed one cartridge of intraosseous anaesthetic per appointment.

Anatomical limitations include inadequate bony space between the teeth, a cortical plate of bone that is too thick to perforate, a low-lying maxillary sinus and a horizontally impacted third molar. In addition, the technique cannot be used between central incisors due to the lack of cancellous bone.

This technique should not be used on patients with cardiac disease.

Onset and duration The onset of anaesthesia is immediate. Duration for pulpal anaesthesia is 20 to 30 minutes if a vasoconstrictor is used and significantly less than that if a vasoconstrictor is not used. Intrapulpal Literature Support       – How does this work? CONT’D▼             VanGheluwe, Walton, 1997 Intrapulpal injection: factors related to effectiveness.  Effective intrapulpal injection depends on back –pressure and not on the solution used. Saline worked as well as 2% Lidocaine  What is a local anesthetic?  Local anesthetics are drugs that produce reversible depression of nerve conduction when applied to the nerve fiber.   How do local anesthetics work?   Local anesthetics work by blocking sodium channels The agent, a weak base, is injected as hydrochloride salt in an acid solution – tertiary amine group becomes quaternary and suitable for injection (i.e. dissolves in solution).  Following injection, the pH increases (due to the higher pH of the tissues, which is usually 7.4) and the drug dissociates, the degree of which depends on pKa, and free base is released.  CONT’D▼  Lipid soluble free base enters the axon. Inside the axon the pH is lower (because the environment is more acidic), and re-ionization takes place.  The re-ionized portion enters the Na+ channels and blocks them, preventing depolarization

 

What determines the onset time of action? SPEED OF ONSET IS RELATED TO pKa  The pKa is the pH at which the drug is 50% ionized and 50% unionized. Ionized drugs are poorly lipid soluble (e.g. morphine compared to fentanyl – the former has a much slower time of onset of action).  Cont’d The closer the pKa is to local tissue pH (usually 7.4), the more unionized the drug is, or, the higher the pKa, the more ionized. Because all local anaesthetics are weak bases, those with a pKa near physiological pH (7.4) will have more molecules in the unionized lipid soluble form (e.g. lignocaine) -> more rapid onset of action. Importance: lower pKa -> better absorption into nerve tissue  higher pKa -> more effective blockade withierve  What determines the duration of action of a local anesthetic? DURATION OF ACTION IS RELATED TO PROTEIN BINDING  The more highly protein bound the drug, the longer the duration of action. More highly bound drugs probably bind for longer to neuronal membrane proteins. The protein probably provides a depot for maintenance of neural blockade. What determines the potency of a local anesthetic?  •        

 POTENCY IS RELATED TO LIPID SOLUBILITY   Highly lipid soluble drugs readily cross membranes, the higher lipid partition coefficient, the more potent and longer DOA of the drug eg. Prilocaine 0.9, Lignocaine 2.9, Bupivicaine 28.   Anesthetic Failures – Hargreaves , Keiser 2002 – Endodontic Topics, Vol. 1, Local Anesthetic Failure in Endodontics 30 – 80 % Failure rate in single carpule, IAN’s with a tooth with irreversible pulpitis.   CONT’D▼  Anatomic causes – variations in skeletal and neuroanatomic variations                    a. Needle deflection Acute tachyphylaxis (reduced responsiveness) Effect of Inflammation on local tissues (pH) Infected tissues have local pH decrease and local anesthetics are less effectve alkalinisation of the solution (by adding bicarbonate)- makes it more effective. By elevating tissue pH it raises the     base-cation ratio (brings the pH & pKa closer together) and increases absorption of the local anesthetic into nerve into the nerve tissue. Effect of Inflammation on blood flow – vasodilation causes reduction in concentration Effect of Inflammation oociceptors – allodynia Effect of Inflammation on central sensitization Psychological factors   Lip test for anesthesia – wrong way to determine extent of anesthesia  Why? Touch and proprioception are mediated by A-beta fibers. Pain perception is mediated by C and A-delta fibers.  Local anesthetics block the heavily myelinated A-beta fibers and the lightly myelinated A-delta fibers at much lower concentrations than unmyelinated C fibers.  The C fibers are the pain receptors! So you can have a numb lip but not be fully anesthetized nerve fibers in pulp! 

   “ MANDIBULAR LOCAL ANAESTHESIA” A CLINICAL COMPARISION OF THREE TECHNIQUES Abstract Inferior dental anaesthesia via the direct intraoral approach, mandibular conduction anaesthesia via extraoral landmarks(Gow-Gates) and mandibular conduction anaesthesia via the tuberosity approach( Akinosi) were evaluated using pain during injection, aspiration test, pinprick, depth and frequency of anaesthesia, onset and duration of anaesthesia. 120 patients of both sexes, aged from 16 years to 50 years, undergoing mandibular molar tooth extraction were included. They were randomly designated into 3 groups with regards to the applied technique of mandibular anaesthesia. Each patient was given injection of 2 ml of 2% lignocaine with adrenaline (1:80,000) using 2ml disposable syringes and a 25 gauge, 1.5 inch needle. Classical inferior nerve block showed greater incidence of pain among the applied techniques. Positive aspiration was most frequently observed with classical inferior nerve block. The onset of anaesthesia was found to be slower with Gow-Gates technique while duration of anaesthesia was longer. Mandibular conduction anaesthesia via the tuberosity approach did not show any particular advantage over the other two techniques in this study. After using Gow-Gates method, we found that the Gow-Gates technique is a highly successful alternative to the conventional inferior nerve block with regards to increased success rate, constancy of landmarks, decreased positive aspiration rate, decreased incidence of complications such as trismus, the advantage of one injection to anaesthetize a greater area supplied by the mandibular nerve, longer duration of anaesthesia and less amount of pain experienced during injection.

Introduction Classical inferior dental anaesthesia is a routine block injection administered regularly in dental practice in children and adults undergoing exodontia, endodontic procedures, minor oral surgical procedures etc. A dental professional encounter a series of obstacles performing a classical inferior dental anesthesia procedure such as non-cooperation from the patient during intraoral approach , pain during injection, longer duration of onset of action, post injection truisms, limited mouth opening as a result of dent alveolar abscess or space infection etc. Unfortunately it also proves to be the most frustrating, the one with the highest percentage of clinical failures (approximately 15%-20%) even when administered properly 1. To encounter the difficulties sometimes observed in achieving inferior dental nerve block, various methods of anesthesia have been suggested, which claims to be superior over the conventional direct method of classical inferior alveolar nerve block. Alternative techniques have been introduced and adopted for circumventing some of the problems encountered with the classical inferior alveolar nerve block. They include the Gow-Gates technique introduced in 1973 and the Akinosi technique introduced in 1977.2,3 There has been considerable controversy as to whether the alternative techniques match the reliability and efficiency of the classical inferior alveolar nerve block. This study has been laid down in an attempt to evaluate the merits and demerits of the three techniques in a randomly selected series of patients undergoing extraction of mandibular permanent molar tooth.

Materials and Methods: 120 patients of both sexes, aged from 16-50 years, undergoing extraction of grossly decayed mandibular first molar tooth were selected from the outpatient door of Institute of dental sciences, Bhubaneswar, India. They were randomly designated into 3 groups with regards to the applied technique of mandibular anaesthesia. Each patient was given injection of 2 ml of 2% lignocaine with adrenaline (1:80,000) using 2ml disposable syringes and a 25 gauge, 1.5 inch needle. The sites of penetration of the needle were dried with sterile gauze and topical antiseptic was applied for all patients. The techniques applied were as follows: Classical inferior nerve block via intra oral approach; mandibular conduction anaesthesia via extra oral landmarks (Gow-Gates); and via the tuberosity approach (Akinosi). All the techniques were performed by a single investigator and assessed by a single examiner who was unaware of the technique used for the patient.

Clinical assessment Clinical criteria for the assessment of the applied techniques were as follows: pain during injection; aspiration test; pinprick test; onset and duration of anaesthesia; depth and frequency of anaesthesia. After insertion of the needle, aspiration was performed and the anaesthetic solution was injected. The patient was instructed to inform examiner of the beginning of numbness of the lower lip, which was regarded as the onset of anaesthesia. 15min later, anaesthesia of the tissue innervated by the sensory oral branches of the mandibular nerve was tested using a pinprick on the following areas of the corresponding side: the lower lip; skin of the cheek 2cm laterally from the angle of the mouth; buccal mucosa adjacent to the lower first molar; and the dorsal side of the tongue. Insensitivity to a pinprick was assigned 0, incomplete sensation and definite sensation were assigned 1 and 2 respectively. During dental extraction, the patient was observed and the occurrence of pain if any was noted according to the severity as mild, moderate, and severe as experienced by the patient. The need for further anaesthesia was also noted. This provided the information on the depth of anaesthesia. In order to estimate the frequency of anesthesia, patients who did not experience numbness of lip or who had severe pain at the commencement of the extraction procedure were counted as failures. In order to determine duration of anesthesia, patients or patients parent were asked to record the exact time when the anesthesia of lower lip wore off. The results were then tabulated and statistically analyzed using Chi square test(x2). Results In our study, evaluation of pain experienced during injection suggested that classical inferior nerve block had greater incidence of pain in respect to Gow-Gates and Akinosi technique. [Table-1, Graph-1] Aspiration tests were positive in 19% of total cases. Positive aspiration was encountered mostly in classical inferior alveolar nerve block technique and the least in Gow–Gates technique. Pinprick test for the inferior alveolar nerve revealed that the tissue insensitivity was more in Gow-Gates technique as compared to other techniques. Pinprick test in the areas innervated by the lingual nerve, Buccal (ext) Buccal (int), the tissue insensitivity was more in classical inferior alveolar technique as compared to other techniques. The pinprick test done along the innervations of buccal nerve(ext) for classical technique presented with 97.5% of tissue insensitivity and 2.5% with incomplete sensation, Gow-Gates presented with 87.5% of tissue insensitivity and 12.5% with incomplete sensation and Akinosi technique presented with 77.5% of tissue insensitivity and 22.5% with incomplete sensation to pinprick . Along the innervations of buccal nerve(int) values for pinprick test for classical inferior alveolar nerve block is 97.5% of tissue insensitivity and 2.5% with incomplete sensation, Gow-Gates technique presented with 90% of tissue insensitivity and 10% with incomplete sensation and Akinosi technique presented with 95% of tissue sensitivity and 5% of incomplete sensation to pinprick . .[Table2- Graph-2]. The highest incidence of successful anaesthesia was recorded with Gow-Gates technique (92.5%) followed by Akinosi technique (90%) and Classical inferior nerve block (72.5%) . Onset of anaesthesia recorded with classical inferior alveolar nerve block technique was 2.15min. Onset of anesthesia as recorded for Gow-Gates and Akinosi technique were 3.85minutes and 2.78minutes .

The onset of anaesthesia was found to be slower with Gow- Gates technique in comparison with the other two technique. Duration of anaesthesia was longer in Gow-Gates technique with 69.3minutes while in Akinosi and Classical technique duration of anesthesia were recorded as 54.2minutes and 45.83minutes respectively. .[Table- 4, graph-4] No complications were encountered during the study, except that one patient who received classical inferior alveolar nerve block had post-extraction trismus where the patient had undergone atraumatic extraction of the lower first molar Discussion Inferior alveolar nerve blocks are routine procedures in dental practice, failure to achieve satisfactory levels of anesthesia often occurs mostly because of anatomical variations or faulty technique. Anatomical variations in the shape and size of the mandible may make accurate location of the mandibular fossa difficult.

The width of the ascending rami and their divergence determine the position of the mandibular foramen, which varies accordingly from one individual to another4. In addition, failure to achieve anesthesia may also be due to a number of other factors like inadequate dosage of the anaesthetic solutions or presence of supplementary or accessory innervations which may together account for increase in failure of inferior alveolar anaesthesia2. As a result of these difficulties, a variety of methods have been suggested for mandibular anaesthesia, with superior results over the conventional direct inferior alveolar nerve block technique. Complete satisfactory anesthesia has been reported in literatures with a frequency of more than 96% with Gow-Gates technique5. Similar results were also reported with Akinosi technique2. In our study, similar results were reported, where in Gow-Gates technique satisfactory anaesthesia was achieved in 92.5 % of cases followed by Akinosi technique with 90% and Classical technique with 72.5%. The significance of performing an aspiration before deposition of anaesthetic solution is to eliminate vascular accidents. The most frequent chances of positive aspiration reported amongst intraoral injections were with the inferior alveolar nerve block at the rate of 10-15%. Malamed S F indicate a very low incidence of aspiration with Gow-Gates6 technique and similar value for Akinosi technique by Todorovic and colleagues8.

Our results also reported less chances of positive aspiration with Gow-Gates and Akinosi technique as compared with classical technique which deposit anaesthetic solutioear the mandibular foramen. The results concerning pain during injection were almost identical for all techniques. Experience of pain is unpredictable and perhaps valid judgement differentiating various techniques. In our study we found pinprick test to be a very reliable method for estimation of anaesthesia achieved. The highest values of inferior alveolar nerve anaesthesia were achieved by Gow-Gates technique while values of lingual and buccal nerve anaesthesia were achieved by classical technique.

With regards to onset of anaesthesia, the slowest onset of anesthesia in our study was accounted for Gow-Gates technique in comparison with other methods. Duration of anaesthesia was longer in Gow-Gates technique. From our study we concluded that the Gow-Gates technique is a highly successful alternative to the conventional inferior nerve block with regards to increased success rate, constancy of landmarks, decreased positive aspiration rate, decreased incidence of complications such as trismus, the advantage of one injection to anaesthetize a greater area supplied by the mandibular nerve, longer duration of anaesthesia and less amount of pain experienced during injection.

Conclusion Classical technique is the most commonly used technique in dental practice. Classical technique has got its own limitation like delayed onset of action, proper positioning of needle and in trismus or limited mouth opening which creates unfavourable condition for the operator to achieve profound anesthesia . Therefore, other techniques has to be explored to achieve inferior dental anesthesia. In our study all the three techniques showed a high rate of success in achieving mandibular anaesthesia. However, the area anaesthetized varied drastically. Maximum area was anaesthetized with the Gow-Gates mandibular nerve block. Therefore, this block can be reserved for cases where a large area of the mandible is involved for surgical procudures. Gow-Gates technique is easy to learn and can be used on a routine basis. The Akinosi technique, despite the decreased visibility, also gave high success rate. Though a variety of mandibular nerve block anaesthesia techniques are available, this study focuses that, these three commonly used techniques are almost equally effective and can be used in situations which necessitate the particular technique. olar nerve block   The Akinosi technique  This method, which is also known as the Vazirani-Akinosi closed-mouth technique, is useful when conventional block anaesthesia fails (fig. 2a,b). It is simpler than the Gow-Gates method, and uniquely for intra-oral approaches to the inferior alveolar nerve, it does not rely upon contacting a bony end-point.

The patient has the mouth closed and the syringe, fitted with a 35 mm needle, is advanced parallel to the maxillary occlusal plane at the level of the maxillary muco-gingival junction. The needle is advanced until the hub is level with the distal surface of the maxillary second molar, by which stage it will have penetrated mucosa at a higher level than with the direct approach to the nerve. At this point a cartridge of solution is deposited.

    The Gow-Gates and Akinosi techniques are both ‘high’ methods of blocking the inferior alveolar nerve; both anaesthetise the lingual nerve. In addition the Gow-Gates method will block conduction in the long buccal nerve (occasionally this also happens with the Akinosi technique).  The Gow-Gates and Akinosi methods are best reserved for those cases where the conventional block methods fail as they can produce more complications than the standard approach. The higher the needle is inserted the closer it is to the maxillary artery and the pterygoid plexus. Contacting the maxillary artery can cause pain and produce blanching because of arteriospasm, laceration of vessels in the pterygoid plexus can cause an alarming haematoma which is controlled by firm pressure but may produce post-injection trismus which may last for weeks.  Other methods of anaesthetising man-dibular teeth include infiltration anaesthesia, incisive and mental nerve blocks, intraligamentary (or periodontal ligament), intra-osseous and intra-pulpal methods. Infiltration anaesthesia  Buccal infiltration anaesthesia in the mandible can be effective in some areas. Indeed in children this may the preferred technique when treating the deciduous dentition.8 In adult patients buccal infiltrations may be effective in the mandibular incisor region. Mental and incisive nerve block  When treating the lower premolar and anterior teeth a mental and incisive nerve block may overcome a failed inferior alveolar nerve block. When using this method 1.5 ml should be injected in the region of the mental foramen which is often located between the apices of the lower premolars (available radiographs can be used to accurately localise the foramen). Intraligamentary and intra-osseous anaesthesia  These techniques rely on the same mechanism to achieve anaesthesia, namely deposition of solution in the cancellous bone of the alveolus. The intraligamentary method gains access to the cancellous space by the periodontium, the intra-osseous technique by way of a perforation through the buccal gingiva. They can be used in either jaw. Intraligamentary anaesthesia  This may be used both as a primary or a secondary technique. It has limitations as a principal method of anaesthesia (such as variable duration) but has been used to overcome failed conventional methods.9, 10  The technique is equally effective with conventional or specialised syringes. Glass cartridges are used in this method as the plastic type deform under the pressures produced.11  When administering intraligamentary injections the needle is inserted at the mesio-buccal aspect of the root and advanced until maximum penetration. A 12 mm 30 gauge is recommended although efficacy is independent of needle diameter.9, 10 Ideally the bevel should face the bone although effectiveness is not impaired with different orientations.12 The needle does not penetrate deeply into the periodontal ligament but is wedged at the crest of the alveolar ridge. Around 0.2 ml of solution is injected per root. When using an ordinary dental syringe 0.2 ml is the approximate volume of the cartridge rubber bung. The injection must be delivered slowly, at least 10 seconds is recommended. Rapid injection can lead to tooth extrusion, indeed an inadvertent extraction has been reported as a result of this method of anaesthesia.13  When using the intraligamentary method success is highly dependent upon the presence of adrenaline in the local anaesthetic solution.14 Care must therefore be taken in patients at risk of increased circulating adrenaline levels as solution injected intra-osseously enters the systemic circulation rapidly. Intraligamentary injections produce a significant bacteraemia17 and thus should not be given to patients at risk of infective endocarditis unless appropriate antibiotic prophylaxis has been provided. Intra-osseous anaesthesia  As with the intraligamentary injection this method can be performed using conventional or specialised equipment. Similarly it is more effective when a vasoconstrictor-containing solution is used.18 Modern custom-made equipment however simplifies the technique. Specialised equipment consists of a matched perforator and needle. If the patient has radiographs of the tooth to be treated these are useful in locating the best inter-radicular zone for anaesthetic injection. If it is not already anaesthetised the gingiva in the area of perforation is infiltrated with a small volume (0.1 ml) of anaesthetic solution. The region to perforate is within the attached gingiva about 2 mm below the gingival margin of the adjacent teeth in the vertical plane bisecting the interdental papilla.The perforator is fitted to a standard dental handpiece and advanced through the buccal cortex until the unmistakable drop into the cancellous space is experienced. The perforator is removed and the small 6 mm 30 gauge needle is advanced through the defect into the cancellous bone where 0.2–0.5 ml of solution is administered slowly. Although there are aspects which preclude intra-osseous anaesthesia as a primary technique it is a useful adjunct to block anaesthesia.19 Intra-pulpal anaesthesia  A technique of anaesthesia that can be useful in endodontics and oral surgery is the intra-pulpal method. Unlike intra- ligamentary and intra-osseous techniques this method achieves anaesthesia as a result of pressure. Saline has been reported to be as effective as an anaesthetic solution when injected intra-pulpally.20 The method is as follows. When a small access cavity is available into the pulp a needle which fits snugly into the pulp should be chosen. A small amount (about 0.1 ml) of solution is injected under pressure. There will be an initial feeling of discomfort during this injection, however this is transient and anaesthetic onset is rapid. When the exposure is too large to allow a snug needle fit the exposed pulp should be bathed in a little local anaesthetic for about a minute before introducing the needle as far apically as possible into the pulp chamber and injecting under pressure.

 

Surveys were sent to Harvard School of Dental Medicine students and graduates from the classes of 2000 through 2006 to determine their current primary means of achieving mandibular anesthesia. Orthodontists and orthodontic residents were excluded. All subjects received clinical training in the conventional inferior alveolar nerve block and two alternative techniques (the Akinosi mandibular block and the Gow-Gates mandibular block) during their predoctoral dental education. This study tests the hypothesis that students and graduates who received training in the conventional inferior alveolar nerve block, the Akinosi mandibular block, and the Gow-Gates mandibular block will report more frequent current utilization of alternatives to the conventional inferior alveolar nerve block than clinicians trained in the conventional technique only. At the 95 percent confidence level, we estimated that between 3.7 percent and 16.1 percent (mean=8.5 percent) of clinicians trained in using the Gow-Gates technique use this injection technique primarily, and between 35.4 percent and 56.3 percent (mean=47.5 percent) of those trained in the Gow-Gates method never use this technique.

At the same confidence level, between 0.0 percent and 3.8 percent (mean=0.0 percent) of clinicians trained in using the Akinosi technique use this injection clinical technique primarily, and between 62.2 percent and 81.1 percent (mean=72.3 percent) of those trained in the Akinosi method never use this technique. No control group that was completely untrained in the Gow-Gates or Akinosi techniques was available for comparison. However, we presume that zero percent of clinicians who have not been trained in a given technique will use the technique in clinical practice. The confidence interval for the Gow-Gates method excludes this value, while the confidence interval for the Akinosi technique includes zero percent. We conclude that, in the study population, formal clinical training in the Gow-Gates and Akinosi injection techniques lead to a small but significant increase in current primary utilization of the Gow-Gates technique. No significant increase in current primary utilization of the Akinosi technique was found.  Keywords: local anesthesia inferior alveolar nerve block Gow-Gates mandibular block Akinosi mandibular block   In late November 1884, William S. Halsted and Richard J. Hall first achieved neuroregional anesthesia in the mandible by injecting a solution of cocaine in the vicinity of the mandibular foramen.1 Since that revolutionary injection, dentists have possessed the remarkable ability to deliver invasive dental treatment in a pain-free manner and relieve suffering for patients.

 Today, pain management is central to the success of any dentist. Indeed, many patients choose their provider based on perceived ability to deliver painless dentistry.   To achieve mandibular anesthesia, most dentists in the United States use an injection technique targeting the mandibular sulcus, similar to the technique described by Jorgensen and Hayden in 1967.2 This injection remains a proven method for delivering local anesthesia in a safe manner with minimal discomfort to the patient, and it usually represents one of the first clinical skills students learn in dental school. However, there are several disadvantages associated with the standard inferior alveolar (IA) nerve block.

One limitation of the Jorgensen technique is that it relies on the presence and identification of anatomical landmarks such as teeth, the pterygomandibular raphe, and the retromolar pad. Malamed identifies the inferior alveolar nerve block as the injection with the highest clinical failure rate, which he reports to be 15 to 20 percent when properly administered.3 This high failure rate is often attributed to a high degree of variation in the morphology of the mandibular ramus and the location of the mandibular foramen, but improper technique is the most common reason for failure.4 Specifically, inadequate mouth opening allows the IA nerve to remain in a relaxed state and fails to bring the nerve into close approximation with the medial wall of the ramus. Improper anterior, posterior, or inferior placement of the needle also commonly leads to failure. Because the target for the conventional IA block is very near the neurovascular bundle, this technique also has a high frequency of positive aspiration, and intravascular injection can occur.5 Furthermore, the standard block often fails to anesthetize branches of cranial nerve V3 that originate proximal to the injection site and provide accessory innervation to the mandibular teeth. The relatively distal location of the injection also leads to lack of anesthesia of soft tissues posterior to the mental foramen.   In the 1970s two alternatives to the standard IA nerve block were introduced. In 1973, George A.E. Gow-Gates described a novel approach to mandibular anesthesia in which the anesthetic solution is injected just anterior to the head of the mandibular condyle at maximal opening. Gow-Gates developed this technique in 1947, after becoming dissatisfied with the reliability of the conventional mandibular block.5 The Gow-Gates method of delivering anesthesia provides several decided advantages.

Most importantly, Gow-Gates used the technique clinically for thirty years and reported a 99 percent success rate.6 Watson and Gow-Gates reported that this mandibular block technique consistently yields a higher percentage of clinically excellent anesthesia than do conventional techniques.7 Malamed later independently reported a 95 percent success rate using the Gow-Gates technique.8 Because of the relatively proximal location of the injection, the Gow-Gates technique blocks virtually the entire distribution of the mandibular nerve.

 This technique also rarely results in positive aspiration and is independent of the anatomy of the inferior portion of the ramus, the mandibular foramen, and the lingula. A recognized disadvantage of the Gow-Gates technique is slower onset of anesthesia, which can take from five to seven minutes.8  A third technique for mandibular anesthesia was introduced by Akinosi in 1977.9 The Akinosi mandibular block is administered while the patient is in a closed-mouth position. The needle is positioned at the level of the maxillary marginal gingiva, parallel to the maxillary occlusal plane.

The syringe is advanced posteriorly, and the needle penetrates approximately 2.5 cm to 3 cm into the soft tissues in the embrasure between the mandibular ramus and the maxillary tuberosity.9 Like the Gow-Gates technique, the Akinosi block delivers anesthetic more proximally than the conventional block, leading to a larger area of anesthesia and a reduced chance that accessory innervation will cause failure. The Akinosi technique, like the Gow-Gates injection, blocks the long buccal nerve, obviating the need for a separate injection.

This technique boasts success rates similar to those achieved with the Gow-Gates method. Akinosi reported a 93 percent first injection success rate.9 Additionally, the Akinosi block utilizes a closed-mouth approach, affording a clear advantage when trismus frustrates administration of the injection. Rapid induction of anesthesia represents another advantage of the Akinosi technique. When administered correctly, positive tongue and lip signs are present in forty seconds.9  The advantages associated with the Gow-Gates and Akinosi techniques make them attractive to dental professionals who want to minimize patient discomfort and anxiety. Despite the advantages, most dentists have not embraced these techniques. Some clinicians may avoid the techniques out of fear of increasing the pain associated with the injection, which is the part of dental procedures most anxiety-provoking for the patient.

However, multiple randomized controlled clinical trials have found no significant differences in pain on injection among the three techniques (standard inferior alveolar nerve block, Gow-Gates mandibular block, and Akinosi mandibular block).10,11 One clinical trial found that the Akinosi technique was subjectively most acceptable to the patient.12 Perceived increased risk represents another reason clinicians may reject the alternative techniques. Indeed, some authors fervently oppose the widespread use of the Akinosi and Gow-Gates techniques.13 Isolated cases of temporary paralysis of cranial nerves III, IV, and VI following the Gow-Gates mandibular block have been reported.14,15 This type of complication may result from omission of careful aspiration and failure to inject the anesthetic solution within the target area.14 According to Malamed, the solution should not be deposited unless bone (the lateral aspect of the neck of the condyle) is sounded with the needle when administering a Gow-Gates block.8 Malamed described the use of extraoral landmarks to administer the Gow-Gates mandibular block as a simple procedure and attributed the high success rates achieved with the Gow-Gates technique to the constancy of these landmarks.8  Our review of the literature reveals no studies, prospective or retrospective, that suggest that the Akinosi and Gow-Gates techniques are associated with higher complication rates or more severe complications. In fact, Malamed reported a decreased incidence of trismus with the Gow-Gates technique upon evaluation of 4,275 cases.8 Nonetheless, alternatives to the conventional inferior alveolar nerve block remain, for the most part, absent from formal predoctoral dental training in the United States. Thus, most dental professionals do not utilize the Gow-Gates and Akinosi techniques.

This study tests the hypothesis that students and graduates who received training in the conventional inferior alveolar nerve block, the Akinosi mandibular block, and the Gow-Gates mandibular block will report more frequent current utilization of alternatives to the conventional inferior alveolar nerve block than clinicians trained in the conventional technique only.   One-page surveys were sent to all Harvard School of Dental Medicine (HSDM) students and graduates from the classes of 2000 through 2006. All responses were anonymous, and subjects were informed that completion of the survey constitutes consent to participate. The HSDM Committee on Human Studies reviewed the survey and approved this study with exempt status (Human Studies Docket Number M11456-101).   A total of 212 surveys were mailed. Subjects were asked to classify their gender, professional status, and year of graduation and identify their current primary means of achieving mandibular anesthesia: standard IA block, Gow-Gates mandibular block, Akinosi mandibular block, or another technique. Subjects also reported which of the three injection techniques they used for their very first injection in dental school. For each injection technique, subjects identified the approximate number of injections they provide per week and estimated their success rates. Finally, subjects reported their protocol for management of failure to achieve profound anesthesia. Subjects that indicated use of only the standard IA nerve block were additionally asked to state their reasons for not using alternative techniques.   Of the 212 surveys mailed, ten were returned due to incorrect addresses, leaving 202 potential subjects. Eight of the graduates with inaccurate addresses on file are female; two are male. Of the 202 potential subjects, 117 graduates and students returned surveys. Twenty-three potential subjects indicated a professional status of orthodontist or orthodontic resident and were excluded from the study, leaving a final response of ninety-four subjects. Forty-five percent of the subjects were dental students, and an additional 12 percent were general dentists. No surveys were returned from oral surgeons or prosthodontists.

Table 1⇓ identifies demographic characteristics of subjects.   Demographic characteristics of subjects 

Academic records indicate that all survey recipients received formal clinical training in the standard IA nerve block, the Gow-Gates technique, and the Akinosi technique during their predoctoral education at HSDM, although only 81 percent of subjects reported formal training in all of these techniques as part of their predoctoral education. Fourteen percent of respondents reported training in the Gow-Gates technique, the Akinosi technique, or both during postdoctoral education.   Seventy-two subjects (76.6 percent) reported using the standard IA block for their very first injection in dental school. The corresponding figures for the Gow-Gates and Akinosi techniques were fourteen (14.9 percent) and seven (7.5 percent), respectively. Eighty subjects (85.1 percent) reported using the standard IA block as their current primary injection technique, while eight (8.5 percent) subjects reported using the Gow-Gates technique primarily. Of the eight individuals who primarily use the Gow-Gates technique, five (63 percent) were dental students, one (13 percent) was an oral surgery resident, one (13 percent) was an endodontist, and one (13 percent) did not identify professional status. Interestingly, five (63 percent) of these eight individuals reported that they used the Gow-Gates technique under supervision for their very first injection in dental school. Characteristics of the eight individuals who primarily use the Gow-Gates technique are summarized in Table 2⇓. No respondents reported using the Akinosi technique as a primary means of achieving mandibular anesthesia.   Characteristics of individuals who primarily use the Gow-Gates technique  To examine the relationship between injection technique and professional status, we created cross-tabulations for each alternative technique (Tables 3⇓ and 4⇓). The percentage of clinicians within each professional category that never use the Akinosi technique was 100 percent for most specialties.

Oral surgery residents reported the lowest frequency (33 percent) of never using the Akinosi technique, followed by periodontics residents (56 percent) and dental students (69 percent). For the Gow-Gates mandibular block, only the pediatric dentists and prosthodontic residents had 100 percent of subjects report never using the technique. The percentage of clinicians that never use the Gow-Gates mandibular block ranged from 0 percent to 100 percent among the professional status categories, with no endodontists reporting never using the technique.   To estimate the proportions of respondents who never use the Gow-Gates and who at least occasionally use the Gow-Gates, respectively, we calculated an exact binomial 95 percent confidence interval.

The same calculations were made for the Akinosi technique. All analyses were conducted in Stata 6.0 (Stata Corp., College Station, TX). At the 95 percent confidence level, we estimated that between 3.7 percent and 16.1 percent (mean=8.5 percent) of clinicians trained in using the Gow-Gates technique use this injection technique primarily, and between 35.4 percent and 56.3 percent (mean=47.5 percent) of those trained in the Gow-Gates method never use this technique. At the same confidence level, between 0.0 percent and 3.8 percent (mean=0.0 percent) of clinicians who received training in the Akinosi technique use this injection technique primarily, and between 62.2 percent and 81.1 percent (mean=72.3 percent) of those trained in the Akinosi method never use this technique. Theoretically, zero percent of those who have not been trained in a given technique will use the technique in clinical practice. The confidence interval for the Gow-Gates method excludes this value, while the confidence interval for the Akinosi technique includes zero percent.

  Forty-six respondents (49 percent) estimated a success rate of greater than 90 percent with the conventional IA nerve block, compared to twenty-nine respondents (31 percent) with the Gow-Gates technique and nine respondents (10 percent) with the Akinosi technique. Estimated success rates for the three injection techniques are shown in Figure 1⇓. Only one subject (1 percent) reported never using the conventional IA nerve block, compared to sixty-six subjects (70 percent) for the Akinosi technique and forty-two subjects (45 percent) for the Gow-Gates technique.

The reported number of injections per week for the alternative techniques diminished sharply at the one to ten injections per week category, whereas a significant number of respondents reported ten to twenty, twenty to thirty, or greater than thirty injections per week using the conventional IA nerve block. The estimated numbers of injections per week for the three injection techniques are shown in   The most common protocol reported for management of failure to achieve profound anesthesia was “give another carpule of local anesthesia using the same technique” (70 percent).

This response was reported at a much higher frequency than the second most commonly reported protocol, “change to Gow-Gates and give another carpule of local anesthesia” (14 percent). The reported protocols for management of failure to achieve profound anesthesia are summarized in Table 5⇓.  Reported protocol for failure to achieve profound anesthesia  Finally, subjects who indicated that they use only the standard inferior alveolar nerve block were asked to state their reasons for never using an alternative injection technique. Responses are summarized in Table 6⇓. Some subjects provided multiple reasons. The most frequently reported reasons for not using alternative techniques were “most comfortable giving the standard injection” (31 percent) and “no need for alternative due to success with the standard injection” (30 percent).    A major limitation of this study is that all subjects received training in all three injection techniques of interest: the standard inferior alveolar nerve block, the Gow-Gates mandibular block, and the Akinosi mandibular block. Ideally, a comparison group would have been available in which the dental professionals received training in only the standard injection. Such a study design would allow hypothesis testing using a χ2 test. Because it was not practical to locate enough dental professionals completely unfamiliar with any alternative mandibular injection technique, we analyzed our data by calculating the 95 percent confidence intervals for the Gow-Gates and Akinosi techniques.   Because the 95 percent confidence interval for the Gow-Gates method excludes zero percent, we reject the null hypothesis that students and graduates who received training in the conventional inferior alveolar nerve block, the Akinosi mandibular block, and the Gow-Gates mandibular block will report equivalent current utilization of alternatives to the conventional inferior alveolar nerve block compared to clinicians trained in the conventional technique only. The 95 percent confidence interval for the Akinosi method does include zero percent, indicating no significant increase in current utilization compared to clinicians trained in the conventional IA nerve block alone. We fail to reject the null hypothesis for the Akinosi technique.   Despite the reported advantages of the Gow-Gates and Akinosi techniques, the findings from this study indicated that only a small percentage of clinicians trained in these injection techniques choose to use them as their primary means of establishing mandibular anesthesia and a large percentage completely abandoned these techniques.   Several factors account for the widespread lack of enthusiasm for alternatives to the standard IA block. Predoctoral programs that include the Gow-Gates and Akinosi techniques in the dental curriculum usually de-emphasize these alternatives due to lack of familiarity among the majority of the faculty. Students tend to view the alternative injections as heroic measures to consider if the standard block fails, and they feel an aversion toward using alternative injections for fear of criticism from their instructors.  

 Few clinicians are willing to stray from the conventional inferior alveolar nerve block they learned in dental school. As dentists gain clinical experience, they learn to manage IA nerve block failures, usually by additional injections (see Table 6⇑). Some clinicians switch to the Akinosi or Gow-Gates block in the event of standard IA block failure. Many dentists repeat the conventional injection after repositioning the needle. In either case, the dentist must revisit the injection, which is the portion of the procedure that patients commonly report as anxiety-provoking. The significantly higher success rates of the Akinosi and Gow-Gates techniques can potentially reduce anxiety for many patients by reducing the need for additional injections.   Norms within professional groups seem to represent another factor influencing the use of alternative injection techniques.

For example, 100 percent of endodontists who responded to the survey indicated that they use the Gow-Gates technique at least occasionally, and 67 percent of endodontic residents indicated the same. Endodontists possibly feel they need alternative injection techniques to achieve adequate anesthesia for their patients.   Current instruction in the Akinosi and Gow-Gates mandibular block techniques in predoctoral dental education does not generally translate into widespread and routine use of these techniques in clinical practice. Possibly, lack of reinforcement following the initial training leads to disuse of the alternative techniques.   Dental schools could dramatically increase the number of graduates using the Gow-Gates and Akinosi techniques through a few simple and inexpensive changes.

The first barrier to the use of these alternative injections techniques is lack of familiarity among the faculty. Providing instructors with a seminar to refresh their skills in the Akinosi and Gow-Gates blocks could diminish this phenomenon. Additionally, requiring students to pass an examination that tests for competency would ensure that all students have the skills necessary to properly administer the injections. Having these skills, students could then assess all three injection techniques and select the one that consistently provides excellent clinical anesthesia.

Finally, dental schools should ensure that students fully understand the reported advantages and disadvantages to the alternative injection techniques.   If dental educators accept the reported advantages to the Gow-Gates and Akinosi injection techniques, then conferring these skills on dental students seems a worthwhile endeavor. Indeed, if students do not learn the alternative techniques during their pre-doctoral education, they are unlikely to ever learn the skills unless they choose to specialize in endodontics or oral surgery. However, dental schools are faced with the difficult challenge of bringing students to a level of clinical competency in only four years. The addition of any content to the curriculum, especially content not essential to reaching an acceptable level of competency, is appropriately met with skepticism and resistance. In our view, inclusion of alternatives to the conventional IA nerve block in predoctoral education can be accomplished efficiently, and the benefits of such training to clinicians and their patients justify the additional expenditure of resources.  

 I come across many patients who have some sort of complaints about their experience with dental anesthesia. I have tried to compile those in a way which can be helpful for you to refer to.

 The common problems related to dental anesthesia can be summarized as follows:  1. The last time that you got an injection, you were numb for hours. Why? Is that normal?   Yes, though rare, it can happen. Getting an area numb (anesthetized) is a clinical skill that dentists or even anesthesiologists acquire over the years through clinical practice. The degree and duration of anesthesia depend on couple of factors:   a)The body metabolism. Anesthetic gets metabolized slowly in some individuals. On the other hand, if you drink a lot of coffee, the anesthesia will wear off rather quickly.

The anesthetic can get metabolized very quickly also in patients with hyperthyroidism with higher BMR (Basal Metabolic Rate).   b) Dentists have to learn the anatomical landmarks and based on that they administer the anesthetic. There is no set measurement for selecting the location for the injection.   For example, it is not that they go 10 mm behind the molars to give the injection, because it depends on your built. The measurements change depending on what size jaw bones you have. Also the individual variation of the position of the nerves play a role.   Therefore, as a result, each time you can get varied response with the same kind of injection. At one time the desired numbness can be achieved which will wear off within a reasonable period of time. But the next time the dentist may end up placing it too close to the nerve. Because the injection is given by assessing the approximate location of the nerve, it is possible that in your case the dentist’s injection could have been very accurate and the anesthetic was placed in close proximity to the nerve producing profound and prolonged anesthesia.   c) The type of anesthetic used. Articane HCl can produce a longer effect compared to that of Xylocaine HCl.

You have to remember that the effect is temporary. Even if it takes a little longer than the previous visit, it is usually still within reasonable and normal limit.  2. The last time the dentist could not get you numb and you felt the pain for a long time? Is that normal?   Yes, it is normal. It should not happen but it can happen. A dentist usually gives injection and allows a reasonable amount of time for the anesthetic to be effective. As explained before, the precise location for the injection can change depending on your built.

Also the individual variation of the position of the nerves plays a role. In some cases, there can be additional or accessory nerves supplying the area. As a result with the same kind of injection each time you can get different responses. Because the injection is given by assessing the approximate location of the nerve, one time the dentist can get the desired numbness which wears off within a reasonable period of time. But the next time the same kind of injection may not effectively anesthetize all of the branches. 

 The best thing is to communicate with your dentist. As soon as you feel any discomfort, raise your hand. Do not jump. Remember, the dentist is working in your mouth with a sharp drill! A dentist who is compassionate about his/her patients will definitely stop and add more anesthetic to achieve the desired numbness.  Note:    It is not uncommon to get a burning sensation right when the anesthetic is administered. You may want to ask for the topical (surface) anesthetic gel a few minutes before the anesthetic is administered to make it little better.  3. The injection that your dentist gives you in the roof of the mouth hurts. Why? 

 The tissue of the roof of the mouth (palate) is thin and firmly attached to the underlying bone. It has a rich nerve supply. So, when the anesthetic is delivered into that area, it stretches the tissue and you feel the intense pain. Unfortunately, very little can be done to reduce that discomfort. Sometimes though Articane HCl (Septocaine) can be used instead of Xylocaine. It penetrates the bone more eliminating the need for a palatal injection, provided the work that is needed is not too involved.  4. When the dentist gave you an injection, you got a bruise in your face exactly in the area that corresponds to that tooth. Is that normal?   Yes. It can happen rarely and can still be normal. When an injection is given it pierces through the layers of muscles that are rich in blood supply. It always bleeds when an injection is given (usually you can taste the blood once the injection is given) but it may occasionally become visible externally if the bleeding takes place closer to the outer layer of the facial muscles. Also, it can get more noticeable, if you’re fair in complexion.  5. When the dentist gave you an injection, your vision became blurred or you were seeing double. Is that normal? Did he do anything wrong?   No, the dentist did not do anything wrong.

Again, it depends on the accuracy of the injection. The 5th Cranial Nerve or the Trigeminal Nerve splits into three divisions after emerging from the cranium (skull):   a) The top branch (Ophthalmic Division) supplies the eyes among other things.   b) The middle branch (Maxillary Division) supplies the top teeth and other tissues in the upper jaw (the Maxilla), and,   c) The third branch (Mandibular Division) supplies the bottom teeth and other tissues in the lower jaw (Mandible).   If the dentist administers the anesthetic in the back where the main trunk splits into these three branches, you can feel the anesthetic effect also in your eye on the same side. It is normal.  Note: 

 For the same reason, you can feel referred pain in the top teeth due to a painful bottom tooth and vice versa.  6. Your muscles hurt after the filling was done. Why?   When anesthetic is administered, the needle pierces through the muscle(s). You may not always feel it because it depends on which muscles are being subjected to trauma.

If it is a muscle that is not often used, you may not feel unless you press on it. The discomfort usually is transient and goes away within days. But if it is a muscle that has to work hard when you chew food or smile, you may feel it more. If you’re a bruxer, you will keep on overworking your muscles, thereby delaying the healing. In that case, the discomfort can be there for a significant period of time.  7. You fell sick when your dentist gave you the injection. It felt like your heart was ‘racing’. You were experiencing palpitation. Why?   The anesthetic most commonly used at the dentist’s office contains epinephrine among other active chemical agents. It is used to constrict the blood vessels to reduce hemorrhage locally and prolong the anesthesia. But at the same time, it can cause an increase in the heart rate. If you experience such problem inform the dentist right away. Your records will be updated to avoid such unpleasant reaction in the future.

If you have had such experience before, don’t forget to include that in the health history when you first go to a dentist’s office. There are alternate anesthetics available, which do not contain epinephrine.  Research findings:   Oral submucosal injection of 40 micrograms of epinephrine accelerates the cardiac performance, with little change in blood pressure and heart rate.

 Note:   You should also have a decent meal before getting the dental procedure done. However, you should not eat anything before a procedure that requires the administration of intravenous anesthetic (I/V sedation). For example, for the extraction of wisdom teeth.  Pharmacology of Outpatient Anesthesia Medications Intravenous sedation has a long history of use in oral surgery practice. Oral surgeons have been the historical leaders in the development of office-based ambulatory anesthesia practice.

The development of newer intravenous agents and techniques have led to the increased acceptance of these practices as being safe and cost effective. Currently, the vast majority (> 70%) of surgical procedures are performed on an ambulatory basis, and at least 20% of surgical procedures are performed with office-based sedation or general anesthesia. While it is neither possible nor the intention of the authors to present the full scope of anesthetic medications including emergency medications in this chapter, we will review the pharmacology of many agents used in office-based sedation and general anesthesia practice. Where applicable the use of these agents in oral surgical practice is highlighted. Pharmacodynamics and Pharmacokinetics Pharmacodynamics Pharmacodynamics is the study of the pharmacologic actions and clinical effects of a drug in the body.1 The clinical response of most anesthetic and sedative medications derives from their actions in the central nervous system (CNS).

At a cellular level the most frequent mechanism by which drugs exert their pharmacologic effects is through interactions with specific protein receptors embedded in cell membranes, which then initiate a specific set of intracellular actions. These protein receptors can be characterized as ion channels or transmembrane receptors. Ion channels allow the passage of specific ions into or out of the cell, including chloride, potassium, sodium, and calcium. Alterations in the intracellular concentration of these ions initiate characteristic cellular effects such as depolarization of a cell membrane or movement of storage vesicles.

Opening of ion channels may be triggered by either changes in membrane voltage or binding by a specific ligand. Voltage-sensitive ion channels open and close depending on cell membrane voltage, whereas a ligand-gated ion channel undergoes conformational changes when a drug or natural ligand binds to it, altering ion channel opening and closing. The -aminobutyric acid (GABA) receptor is an example of a ligand-gated chloride ion receptor. Transmembrane receptors are also ligand regulated and typically rely on second messenger systems to carry out the pharmacodynamic effect.When a specific ligand binds to the extracellular portion of these transmembrane receptors, a conformational change in the domain of the receptor exposed towards the cytoplasm activates either a specific enzyme or a second messenger system.

Second messenger systems, such as G proteins and cyclic adenosine monophosphate, are complex cascades of signaling proteins that, once triggered, will produce the intended effect. An example of an enzyme-activated system is insulin, which binds to its specific receptor, activating an intracellular enzyme called tyrosine kinase, resulting in increased glucose uptake.

Muscarinic acetylcholine (ACh) receptors also use a second messenger cascade involving intracellular calcium. Some lipid-soluble drugs do not engage membrane receptors, but instead exert their pharmacodynamic effect intracellularly via receptors found in the cytoplasm. Hormones and steroid medications cross the cell membrane and bind to cytoplasmic receptors, which then alter cellular functions such as gene transcription.

 A small number of medications may also alter enzyme activity outside of cells, such as anticholinesterase drugs that block the activity of acetylcholinesterase. Drugs are commonly classified as either agonists or antagonists for a specific receptor. Agonist drugs function to exert the normal property associated with receptor activation. GABA A agonists like benzodiazepines activate GABA receptors, allowing an influx of chloride, hyperpolarizing the cell, and reducing neuronal activity, thus promoting the normal activity associated with GABA activation. Antagonist drugs exert the opposite effect of the natural ligand or agonist drug activity. Competitive antagonists bind at the normal ligand-binding site but exert no pharmacologic effect. Instead the antagonist “takes up space” at the binding site, thus blocking agonist drug activity. The higher the concentration of antagonist, the greater the blocking effect.

Agonist activity returns once the antagonist concentration decreases or if additional agonist is administered to overcome the antagonist concentration. Nondepolarizing neuromuscular blockers are competitive antagonists for the acetylcholine receptor. Noncompetitive antagonists do not bind at the ligand site but instead attach to a different location on the receptor, altering the configuration of the binding site and preventing normal ligand binding. Administration of an additional agonist does not affect noncompetitive antagonist activity, as they do not compete for the same binding site. Many pesticides are an example of noncompetitive antagonist agents. Pharmacokinetics Pharmacokinetics is the study of the factors that affect the plasma concentration of a drug in the body, encompassing the processes of absorption, distribution, metabolism, and elimination.1 Commonly identified by the route of administration, such as per oral (PO), intravenous (IV), intramuscular (IM), or inhalation, absorption describes the point of entry of the drug into the body. Orally administered agents undergo first-pass metabolism; PO medications are absorbed by the intestinal mucosa and carried via the portal circulation to the liver where they undergo partial metabolism prior to entrance into the central circulation. This process potentially reduces the plasma concentration of drug that reaches the effector site, such as the CNS. Since the degree of gastrointestinal absorption and first-pass metabolism is unpredictable, PO sedative drugs can have less reliable clinical effects. Most anesthetic agents used in oral surgical practice are delivered intravenously, intramuscularly, or by inhalation. In contrast to oral agents these routes of administration do not undergo firstpass metabolism. Both intravenous and inhalation administration provide direct entry into the central circulation, reaching peak plasma concentration very quickly following drug administration.

Inhalation pharmacokinetics will be discussed in the following section “Inhalation Anesthetics.” Distribution describes the movement of the drug between body compartments. The main factors influencing distribution include the allocation of blood flow to a specific compartment, the concentration gradient of the drug between compartments, the chemical structure of the drug, and plasma protein binding of the drug. Following administration the majority of the drug initially redistributes to the vessel-rich compartments.

This vessel-rich group includes the brain, heart, kidney, and liver, representing 10% of total body mass but 75% of cardiac output. Since the major site of anesthetic agent activity is the brain, early distribution to the CNS results in early anesthetic effects. The transfer of the drug from the central circulation to the brain is also determined by the concentration gradient between the two compartments. A lower concentration in one compartment favors the transfer from a region of higher concentration. Following initial intravenous administration the initial drug concentration in the brain is low relative to the plasma concentration; thus, the drug will rapidly transfer into the brain based on this differential concentration gradient. As the plasma concentration falls by continued redistribution to other vessel-rich organs, and later to less vessel-rich organs such as skeletal muscle (approximately 20% of cardiac output), anesthetic drug not bound to receptors in the brain will transfer back into the central circulation for further redistribution to other tissue sites. As the brain concentration of sedative agent falls, the clinical effects of sedation also decrease. Characteristics of the drug itself affect its distribution throughout the body. Lipophilic drugs readily cross the bloodbrain barrier and cellular membranes, and generally exert their effects rapidly. Likewise lipophilic drugs can quickly exit the CNS, shortening the duration of their effects. Hydrophilic medications either cross very slowly or must be transported by specific mechanisms. The size or molecular weight of the drug molecules influences movement across capillary walls; smaller molecules will cross more readily. The degree to which the drug binds to plasma proteins such as albumin and 1- acid glycoprotein will affect the amount of free drug available to cross into the brain. Most sedative agents are highly plasmaprotein bound.

For example, initial doses of diazepam are 98% bound to plasma protein and unavailable to cross into the CNS. As the free drug plasma concentration decreases through further redistribution, and later metabolism and elimination, plasma–protein-bound drug is released back into the plasma as free drug and is able to cross the blood-brain barrier. In this way drug bound to plasma protein may be thought of as a reservoir of drug that may contribute to prolonged sedative effects. Once plasma-protein binding sites have been filled, an additional consequence is that further administration of small quantities of drug can have profound effects as the majority of the additional administered agent will be free drug that is able to cross the blood-brain barrier.

Careful titration of intravenous agents, especially after initial administration and filling of protein binding sites, is important to avoid oversedation due to this mechanism. Hypoproteinemia secondary to advanced age or severe liver failure can also dramatically increase the concentration of free drug, and dose reduction may be required. As redistribution continues, a fraction of the plasma concentration is delivered to the liver, the primary organ of drug metabolism, undergoing transformation from a lipid-soluble entity to a water-soluble form. There are four main pathways of hepatic metabolism: oxidation, reduction, hydrolysis, and conjugation. Phase I reactions include the first three pathways, converting the drug into a water-soluble metabolite or intermediate form. Phase II reactions involve most forms of conjugation, in which an additional group is added onto the metabolite in order to increase its polarity. Subsequent elimination via the kidney, the main excretory organ, requires hydrophilicity to avoid reabsorption of the excreted drug. Water-soluble drugs and metabolites are eliminated chiefly by the kidney, but also via the bile, lungs, skin, and other organs. Phase I hepatic reactions, including the cytochrome P-450 (CYP-450) group of enzymes which carry out the oxidation and reduction reactions, occur in the hepatic smooth endoplasmic reticulum (hepatic microsomal enzymes). The CYP- 450 group of enzymes has been characterized into several isoforms, including CYP- 3A4, CYP-2D6, and CYP-1A2. The conjugation reaction of glucuronidation is also conducted by the hepatic microsomal enzymes.

The hepatic microsomal enzymes are unique in that certain chemicals and drugs, including those used in anesthesia, can stimulate their activity. This is termed enzyme induction and generally requires chronic exposure of the drug to the enzyme system for at least several days or weeks. An isolated exposure to anesthetic agents is unlikely to induce hepatic enzyme activity. However, if the patient’s daily medications induce hepatic enzymes, then increased metabolism of additional medications is possible. Induction is isoform specific; a coadministered drug will only be affected by enzyme induction if both drugs are metabolized by the same enzyme system. Hepatic microsomal enzymes can also be inhibited by certain drugs, thus reducing metabolism of drugs by a specific enzyme system.

 For example, patients taking cimetidine for treatment of gastric ulcers may experience prolonged residual CNS effects from diazepam, as cimetidine inhibits the hepatic enzymes that normally metabolize diazepam. Various tables have been published which list drugs that are substrates, inducers, and inhibitors of the various cytochrome enzyme systems. Nonhepatic forms of metabolism are important for certain anesthetic medications, and are useful in patients with significant liver or kidney disease. Drugs susceptible to Hofmann elimination spontaneously degrade at body pH and temperature. Ester hydrolysis by nonspecific and specific (eg, pseudocholinesterase) esterases is also less dependent on renal and hepatic functions. Redistribution, metabolism, and elimination reduce the plasma concentration of the drug, increasing the transfer of drug from tissue sites (eg, brain) back into the central circulation for further redistribution, metabolism, and elimination. Different mathematical models involving these processes have been developed that describe the offset of activity of anesthetic agents. The fall of 50% of the plasma concentration of the drug secondary to redistribution is termed the alpha half-life. The removal of 50% of the drug from the body due to metabolism and/or elimination is termed the beta half-life, or elimination half-life.

Offset of clinical effects and awakening from a bolus of an IV anesthetic agent is more dependent on redistribution of the drug away from the brain and is therefore better approximated by the alpha half-life than the beta half-life. In some cases residual CNS effects can be predicted by a long elimination half-life. The beta half-life has more use for orally administered agents and particularly describes central compartment concentration in a one-compartment model. The pharmacokinetics of a continuous infusion of intravenous anesthetic agents may be better described by the context-sensitive half-time. This value represents the time necessary for the plasma drug concentration to decrease by 50% after discontinuing a continuous infusion, depending on how long the anesthetic agent has been administered.2 Figure 5-1 describes the context-sensitive half-time for a number of common anesthetic agents. Currently computercontrolled pumps administer continuous infusions based on a specific amount of drug per time, but the newest infusion pumps can be programmed to calculate and provide target plasma concentrations of an agent to a specified anesthetic or analgesic level. In the future these pumps will likely be integrated with concurrent electroencephalogram consciousness monitoring to individualize anesthetic drug delivery.

Benzodiazepines Benzodiazepines are the most commonly used sedative and anxiolytic medications in oral surgery. Their relatively high margin of safety as compared to other sedativehypnotic medications, in addition to the availability of an effective reversal agent, makes their use attractive during operator-anesthetist procedures in an outpatient setting. Benzodiazepines are composed of a benzene and diazepine ring fused together.3 Agonist agents contain a 5-aryl substitution which is not present on the antagonist reversal agent (Figure 5-2). This structure binds to inhibitory GABA receptors found throughout the brain, particularly in the cerebral cortex. Binding to the GABA A subunit increases the frequency of poreopening in the chloride-gated channel, thus increasing inward chloride flow, hyperpolarizing cell membranes, and reducing neuronal transmission. Characteristics shared by benzodiazepines include sedation, anxiolysis, anterograde amnesia, muscle-relaxing properties, and anticonvulsant activity. Indeed, any intravenous benzodiazepine agonist may be used to suppress acute seizure activity. These drugs do not produce analgesia.

Benzodiazepines are commonly used for preoperative sedation both immediately prior to the procedure and as a sleep adjunct the night before surgery. In clinical practice they are also used for conscious sedation, and at higher doses can produce deep sedation and even general anesthesia. In a nervous patient anxiolysis from benzodiazepines can produce noticeable reduction in blood pressure and heart rate, but these medications have little direct effect on cardiovascular parameters. Given alone in slowly titrated doses, benzodiazepines also have minimal effects on ventilation. Large bolus doses will, however, induce unconsciousness and apnea. Additionally, even smaller doses when given in combination with an opioid can synergistically enhance opioidinduced respiratory depression. Benzodiazepines are metabolized by hepatic enzymes into hydrophilic forms. These metabolites are then excreted by the kidney in urine. Side effects of benzodiazepines are few, but paradoxical excitement, in which patients may become overly disinhibited and disoriented, is a possible complication. Flumazenil is useful in the reversal of paradoxical excitement and benzodiazepine- related respiratory depression. Diazepam Diazepam is lipid soluble and is carried in an organic solvent such as propylene glycol or a soybean oil emulsion. Intravenous injection can be painful, although injecting into a larger vein or pre-administration of lidocaine or an opioid can reduce discomfort. Intramuscular injection is painful and absorption can be unpredictable. Diazepam is still used for intravenous conscious sedation, given in 2.5 to 5 mg increments every few minutes. Onset of sedation occurs in several minutes and recovery from clinical sedation by diazepam is similar compared to midazolam. However, the much longer elimination time of diazepam may contribute to lingering sedative effects. Diazepam can also be given orally (5 to 10 mg) for preoperative anxiolysis and mild sedation. This highly lipid-soluble drug accumulates in fat tissues with slow reentry of very small quantities into the central circulation, leading to an elimination halflife of 24 to 96 hours. Diazepam is also metabolized into two pharmacologically active metabolites, desmethyldiazepam and oxazepam, each with long elimination half-lives as well. The active metabolites and parent drug are partially eliminated in bile and can result inreemergence of sedation several hours after completion of the procedure, due to enterohepatic metabolism. Upon ingestion of a fat-rich meal, bile is released into the gut, and active drug components in the bile are reabsorbed by the intestinal mucosa and undergo first-pass metabolism.

These still active drugs are then re-introduced into the central circulation and into the CNS, resulting in possible resedation. Midazolam Midazolam has an imidazole ring attached to its diazepine ring. The imidazole ring is open, rendering the compound water soluble at pH less than 4, but the ring closes at physiologic pH producing the lipid-soluble benzodiazepine. Midazolam can therefore be delivered in an aqueous solution, rather than propylene glycol, resulting in less pain on intravenous and intramuscular injection. 4 It is 2 to 3 times as potent at diazepam, with a faster onset, much faster elimination, and shorter duration of lingering effects. Its active metabolites are not thought to produce significant sedative effects. Respiratory depression is more of a concern with midazolam than diazepam after bolus intravenous administration. Midazolam is currently more popular than diazepam for intravenous sedation for short oral surgical procedures. For conscious sedation 0.05 to 0.15 mg/kg IV in divided doses is titrated to effect, typically given in 1 or 2 mg boluses every few minutes. Peak effect is seen in approximately 5 minutes. Dosage should be adjusted downward when given concurrently with other medications such as opioids or propofol. An intramuscular injection of 0.5 mg/kg to a maximum of 10 to 15 mg depending on patient age is also possible. As an alternative midazolam may be given orally at 0.5 to 1 mg/kg (maximum 15 mg), usually mixed into a flavored syrup or in a commercially available premixed product; this route may be better accepted by pediatric patients.5 Clinical effect from PO administration will be seen after 15 to 20 minutes in the pediatric patient. Lorazepam Lorazepam is a long-acting benzodiazepine with a slow onset. Its use for PO and IV sedation is therefore limited but is an option for oral preoperative anxiolysis, particularly the night before surgery or for long operative appointments. Dosage for an adult is 0.05 mg/kg, not to exceed 4 mg total. Triazolam Triazolam is only available in an oral formulation as 0.125 mg and 0.25 mg tablets.

This sleep adjunct can be used off-label for anxiolysis and sedation at a dose of 0.25 to 0.5 mg for an adult. It is a very short-acting benzodiazepine and its effects are observed in 30 to 45 minutes with clinically effective sedation lasting from 30 to 90 minutes. Flumazenil Flumazenil is a highly specific competitive antagonist for the benzodiazepine receptor and is used as a reversal agent for benzodiazepine agonists.6 It will reverse benzodiazepine sedation, excessive disinhibition, and the additive ventilatory depression related to benzodiazepines when combined with opioids. Flumazenil is given 0.2 mg IV initially, followed by 0.1 mg at 1-minute intervals as necessary, to a total of 1 mg. In emergency situations, 0.5 to 1 mg or more may be administered in a bolus dose. Reversal effects may take several minutes to manifest.

The effect of flumazenil will last 30 to 60 minutes and may require redosing since agonist drug activity may outlast the reversal effects. Flumazenil should not be administered to epileptic patients using benzodiazepines for seizure control and should be used cautiously with other epileptic patients. Opioids Opioid medications are used in oral surgery primarily for analgesia and mild sedation or euphoria. It is important to note that narcotic medications do not produce amnesia or classic sedation, nor do they induce loss of consciousness or sensation of touch at clinically relevant doses. Patients given opioid medications alone will retain awareness and memory. Instead, opioids are often used in combination with sedative-hypnotic medications such as benzodiazepines and barbiturates to provide analgesia and augment the desired level of anesthesia.

While the term opiate refers to any drug derived from opium, opioid medications include all substances, natural and synthetic, which bind to the opioid receptors. 7 Common opioid medications are shown in Figure 5-3. Endogenous opioids such as endorphins and enkephalins, and administered opioid medications like morphine, bind to opioid receptors located in presynaptic and postsynaptic neurons throughout the CNS as well as in peripheral afferent nerves. Agonist activity at these receptors either modifies or decreases neuronal transmission of pain signals. Several subtypes of opioid receptors (eg, μ, κ, δ) with differential effects have been identified. The μ and κ receptors are predominantly responsible for analgesia, and most clinically used opioids are agonists for the μ receptor. A subset of opioids, termed agonist-antagonist opioids, are agonists at κ receptors and antagonists at μ receptors. Thus agonist-antagonist opioids are contraindicated for patients on long-term opioids, such as those using these agents for chronic pain or those on methadone maintenance for treatment of opioid substance abuse.

Respiratory depression is the most common and pronounced side effect of μ receptor agonists as used in anesthetic practice. This effect can be significantly exacerbated with concurrent administration of other medications such as benzodiazepines, barbiturates, propofol, and other opioids. Respiratory depression is dose dependent, resulting from a decrease inthe respiratory response to arterial carbon dioxide (CO2) levels in the brainstem respiratory centers. Decreased respiratory rate and arterial hypoxemia may result without supplemental oxygen (O2) and appropriate monitoring (eg, pulse oximetry). Opioids are often titrated incrementally to balance the analgesic effect against respiratory depression.

Bradycardia as a direct effect is more apparent with high doses of opioids and is due to centrally mediated vagal response. This effect is common with opioids such as morphine, fentanyl, and the synthetic derivatives, but less common with meperidine. A mild decrease or stabilization of the heart rate may be desirable in patients with cardiovascular disease. Most opioids are metabolized by hepatic enzymes and excreted into the urine and bile.

The exception is remifentanil, which is metabolized by plasma esterases. Opioids suppress the cough reflex and are a common ingredient in cough medicines. These antitussive effects can be beneficial during sedation, especially when used in patients with hyperreactive airways (eg, smokers). However, several opioids can cause the release of histamine and caution should be used when histamine-triggering opioids are administered to an asthmatic patient. Other manifestations of histamine release include a decrease in blood pressure secondary to vasodilation, and pruritus and erythema, especially at the site of injection. Other adverse effects such as nausea and vomiting, constipation, urinary retention, and biliary tract spasm may increase patient discomfort postoperatively, particularly with repeated oral or neuraxial administration.

 These reactions are frequently misinterpreted by the patient and other health care providers as an “allergic” reaction. Morphine Morphine is the standard agent by which other opioids are compared. It has poor lipid solubility and therefore has a slow onset. Peak effect following IV administration occurs in 15 to 30 minutes and the analgesic effect lasts approximately 4 hours. Because of its slow onset and longer duration of activity, it is commonly used in anesthesia for postoperative pain management rather than intravenous sedation. Morphine is normally given in 1 to 2 mg IV increments for postoperative analgesia. Morphine has several notable characteristics. Histamine release from morphine can result in skin flushing and a decrease in blood pressure and may be of concern in an asthmatic patient. Morphine is metabolized by hepatic enzymes into two metabolites that are subsequently eliminated by the kidney.

 One of these metabolites, morphine-6-glucuronide, is more potent than morphine itself, and prolonged opioid effects in patients with renal failure can be significant. Meperidine Meperidine is a synthetic opioid with a relatively rapid onset time and duration of action between 2 and 3 hours. It is used for both intravenous sedation and postoperative pain control.

Meperidine is usually given in 12.5 to 25 mg IV increments titrated to effect. The drug has several identifying characteristics. Like morphine, it also has an active metabolite, normeperidine, which is half the potency of meperidine. When mixed with monoamine oxidase inhibitors, meperidine administration may produce a dangerous excitatory hyperthermic reaction. With repeated dosing, particularly in renally compromised patients, accumulation of normeperidine may lead to seizures.Meperidine is also associated with the release of histamine; thus, appropriate precautions should be taken. Unlike the other opioids it is not associated with bradycardia; its structure resembles atropine and it possesses mild anticholinergic effects such as a mild increase in heart rate (offset by direct vagal stimulation) and xerostomia.Meperidine is commonly used to reduce shivering postoperatively, an action likely associated with partial agonist activity at the κ receptor. Fentanyl Fentanyl is a synthetic opioid, and its high lipid solubility leads to its high potency, rapid onset (1 min), and shorter duration of action (10 to 20 min). Withsuch characteristics fentanyl is a frequent choice for intravenous conscious sedation for short office-based procedures. It is typically given in 25 to 50 μg increments towards a total dose of approximately 1 to 2 μg/kg. It is also given during induction of general anesthesia, both for analgesia and attenuation of airway reflexes during intubation. Fentanyl does not induce histamine release and is therefore not associated with vasodilatory or bronchospastic effects. However, at higher doses, it can cause more pronounced bradycardia than morphine. Fentanyl is a potent respiratory depressant.

At high doses and with rapid bolus administration, fentanyl and other synthetic derivatives have been associated with chest wall and glottic rigidity, making ventilation impossible; there are reports that even lower doses (eg, 100 μg) can trigger this centrally mediated effect. Fentanyl-associated chest wall rigidity is treated with either naloxone or succinylcholine (SCh), and positive pressure O2 and other resuscitation equipment should be immediately available. The incidence of fentanyl rigidity is reduced by a preceding dose of a benzodiazepine or other hypnotic drug. Remifentanil, Sufentanil, and Alfentanil Remifentanil, sufentanil, and alfentanil are synthetic fentanyl derivatives used primarily for analgesia during general anesthesia. Remifentanil in particular is associated with a rapid onset and extremely short duration of action, resulting in a significantly shorter recovery time. Metabolized by nonspecific plasma esterases, its clearance is very rapid and independent of both hepatic and renal functions. It has a very short context-sensitive half-time of 4 minutes with virtually no cumulative effect, even following hours of continuous infusion.

These features make remifentanil ideal for use in a titratable continuous infusion. Of note is the fact that because the actions of this medication are so shortlived, postoperative pain will not be addressed by intraoperative remifentanil, and alternative pain control with another narcotic such as a nonsteroidal antiinflammatory drug (NSAID) or local anesthesia should be considered towards the end of the procedure. Remifentanil is used in a total intravenous infusion anesthetic technique to maintain anesthesia during dental surgery, often in combination with propofol. For analgesia during general anesthesia it is used at 0.25 to 1 μg/kg or 0.5 to 2 μg/kg/min. During sedation the dose ranges from 0.05 to 0.10 μg/kg/min. Remifentanil, like fentanyl, can cause chest wall rigidity and caution should be used during bolus administration. It is also a highly potent respiratory depressant, and even at lower doses, apnea may be pronounced. If spontaneous ventilation is desired the remifentanil infusion is usually titrated to maintain an adequate respiratory rate. None of these synthetic derivatives cause the release of histamine. Sufentanil and alfentanil are shorteracting agents than fentanyl but not as rapid in offset as remifentanil. These agents are commonly used as a continuous infusion adjunct for intubated general anesthesia during cardiac or prolonged surgery, particularly when residual opioid effects are desirable postoperatively. They are not as commonly used for office-based oral surgical anesthesia. Nalbuphine Nalbuphine is the most frequently used intravenous agonist-antagonist opioid. It has a relatively short onset and duration of action of 2 to 4 hours at sedation doses of 5 to 10 mg for the adult patient. Although nalbuphine and other agonist-antagonist opioids do possess a ceiling effect for respiratory depression at higher doses, at equianalgesic and clinically relevant sedation doses, the respiratory depressant effects are similar to μ agonist opioids.

Nalbuphine does not release histamine. Unlike all the other agents noted above which are US Drug Enforcement Agency Schedule II controlled substances, nalbuphine is not currently a scheduled controlled substance and does not require state and federal documentation of use. Naloxone Naloxone is a pure opioid antagonist that is active at all opioid receptor subtypes. It will reverse both the ventilatory depressive and analgesic effects of opioids. It can also be used to reverse chest wall or glottic rigidity from fentanyl and its derivatives. In patients taking opioids chronically (eg, chronic pain management, illicit opioid users, methadone therapy for opioid abuse), naloxone must be used with caution as the antagonist effect may precipitate acute opioid withdrawal and acute congestive heart failure may result. The initial dose is 0.4 to 2 mg IV for acute reversal. Naloxone can also be titrated in 0.04 mg increments when gradual adjustment of mild respiratory depression is required. Because the duration of naloxone activity is 30 to 45 minutes, reemergence of respiratory depression may occur and additional dosing may be needed. Barbiturates Barbiturates are sedative-hypnotic medications that have long been employed as induction agents of general anesthesia. Barbiturates produce sedation, loss of consciousness, and amnesia. These drugs do not provide analgesia and may actually reduce pain threshold at lower doses. Several barbiturates such as IV pentobarbital and oral phenobarbital are commonly used as anticonvulsants for both prevention and treatment of seizures. High doses of any intravenous barbiturate can also suppress acute seizure activity. Barbiturates are derivatives of barbituric acid (Figure 5-4). The characteristics of the individual barbiturate are determined by the side chains attached to the barbiturate ring (Figure 5-5).

For example, sulfur substitution on the no. 2 carbon in thiobarbiturates increases the lipid solubility of these drugs and hence decreases onset of action and duration of activity. The methyl group attached to the nitrogen atom of the ring in methohexital results in a more rapid onset for this oxybarbiturate and increased susceptibility to cleavage, producing a shorter duration than other oxybarbiturates. Barbiturates act on GABA receptors at a specific binding site (different from benzodiazepines), causing the chloride channel to remain open for a longer duration. The increased negative inward flow hyperpolarizes the membrane, decreasing neuronal transmission. Awakening from intravenous barbiturates is dependent on redistribution from the brain.

These medications are metabolized by hepatic enzymes without the formation of active metabolites and are then cleared renally. Because these drugs are highly protein-bound, hypoproteinemia secondary to liver failure or malnutrition increases the plasma concentration of free drug. Chronic use of barbiturates can cause induction of liver enzymes. Barbiturates are also contraindicated in patients with acute intermittent porphyria as they may precipitate an attack. Barbiturates are associated with a dose-dependent decrease in respiratory rate and tidal volume with apnea observed at higher doses. Centrally mediated peripheral vasodilation leads to a transient drop of 10 to 30% in systemic blood pressure, particularly when a full induction dose is administered. This is partially attenuated by a compensatory increase in heart rate as baroreceptor reflexes remain intact. Hypotension is more evident in the elderly or medically compromised, hypovolemic patients.

Thiopental can cause histamine release, which is clinically insignificant with methohexital. Intra-arterial injection of barbiturates causes painful spasm of the vessel from precipitation of barbiturate crystals, which damage the endothelium and may result in occlusion of the artery. At worst, decreased distal perfusion may result in tissue necrosis of a limb or nerve damage and must be addressed immediately. The intravenous catheter should be left in place, IV cardiac lidocaine or procaine (without epinephrine) administered, and the patient should be transported to an emergency department where medications or regional blockade may be given to relieve the spasm and reduce the occlusion. Although also uncommon, venous irritation and thrombosis secondary to crystal formation is also possible with concentrations of barbiturates above 1% methohexital and 2.5% thiopental. These medications are stored in powder form and reconstituted in saline prior to use as sodium salts. The alkalinity of the solutions prevents bacterial growth and ensures a longer refrigerated shelf life of up to 2 weeks for thiopental and 6 weeks for methohexital. Thiopental

Thiopental is an ultrashort-acting barbiturate that is commonly used at 3 to 5 mg/kg IV to induce loss of consciousness for general anesthesia prior to endotracheal intubation. It is associated with a longer recovery than methohexital due to its decreased plasma clearance and is generally not used as a continuous infusion to maintain anesthesia due to significant storage in multiple drug compartments. A 2.5% solution of thiopental is lessexpensive than other induction agents, but when rapid recovery is desired during outpatient anesthesia, other agents such as methohexital and propofol have proven more popular. Thiopental can release histamine, which is a concern in asthmatic patients. Methohexital Methohexital is an ultrashort-acting barbiturate that is commonly employed for outpatient oral surgical procedures, primarily for its more rapid recovery compared to thiopental and its lower cost compared to propofol. As an oxybarbiturate, methohexital is less lipid soluble than thiopental but is associated with a more rapid awakening because of its increased hepatic clearance.8 Psychomotor function returns more quickly with methohexital than thiopental, allowing for earlier discharge following an outpatient procedure. Methohexital is reconstituted into a 1% solution and given at 1.5 to 2 mg/kg IV for induction of general anesthesia.

With these doses blood pressure may drop by up to 35% and heart rate increases up to 40% of baseline. In a common deep sedation technique used in oral surgical practice, 10 to 30 mg increments of methohexital are periodically administered after obtaining baseline conscious sedation with a benzodiazepine and opioid to produce a state of deep sedation for local anesthetic administration and other stimulating portions of dentoalveolar surgery.

Methohexital is associated with involuntary movements such as myoclonus and hiccuping. These excitatory phenomena are dose dependent and may be reduced by prior administration of opioids. Low doses of methohexital can activate seizure foci and should be used cautiously, if at all, for epileptic patients. Shivering upon awakening is also common following methohexital anesthesia. Methohexital exhibits clinically insignificant histamine release. Pentobarbital Pentobarbital is an intravenous shortacting barbiturate with a duration of action of 2 to 4 hours. It is generally used for conscious sedation in doses of 100 to 300 mg, combined with opioids and possibly benzodiazepines, for longer operative procedures.

Cardiovascular effects are more modest than the ultrashort-acting agents. Nonbarbiturate Induction Agents Other medications are available for sedation and induction of general anesthesia. These include propofol, etomidate, and ketamine, all of which can produce unconsciousness but with several differing characteristics from barbiturate medications. Propofol Propofol has become one of the most popular sedative-hypnotic drugs used for ambulatory surgery. Propofol, 2,6– diisopropylphenol (Figure 5-6), is highly lipid soluble and available as a milky white 1% suspension in soybean oil, glycerol, and egg phosphatide. Like benzodiazepines and barbiturates, propofol is thought to interact with the GABA receptor, causing increased chloride conductance and hyperpolarization of neurons. At higher doses propofol can produce amnesia and loss of consciousness.

It is also an anticonvulsant, although spontaneous excitatory movements may be noted following administration.9 Depending on the dose and technique, propofol is used for all levels of sedation and general anesthesia. For induction of general anesthesia a bolus of 1.5 to 2.5 mg/kg IV produces unconsciousness within 30 seconds. In the intermittent bolus technique frequently used for deep sedation in oral surgery, small increments of propofol (10 to 30 mg) are periodically administered after a baseline conscious sedation with a benzodiazepine and opioid is obtained, in order to produce a state of deep sedation for local anesthetic administration and other stimulating portions of dentoalveolar surgery.

Propofol can also be used as a continuous intravenous infusion. 10 The dosages for conscious sedation range from 25 to 100 μg/kg/min, deep sedation from 75 to 150 μg/kg/min, and general anesthesia from 100 to 300 μg/kg/min depending on the use of intubation. The overlap of dose ranges, from conscious sedation to general anesthesia, highlights the lower margin of safety of this drug, especially if the intended level of sedation is conscious sedation. US Food and Drug Administration labeling prohibits use of propofol by those involved in the conduct of the surgical or diagnostic procedure.

Propofol is extensively metabolized by hepatic enzymes. In addition, extensive redistribution and other mechanisms of metabolism and elimination most likely occur, as the rate of propofol clearance from the plasma exceeds hepatic blood flow. This rapid plasma clearance may account for the decreased cumulative effect of this drug in the body, contributing to rapid awakening. The context-sensitive half-time for this drug is short, reaching a maximum of 40 minutes even after 2 to 6 hours of continuous infusion. Contextsensitive half-times are even shorter with brief infusions. Propofol decreases systemic blood pressure by as much as 20 to 40% from baseline through centrally mediated vasodilation. Propofol also blocks sympathetic tone and allows parasympathetic vagal responses to predominate, thereby blunting the reflex tachycardia that wouldnormally be associated with such a drop in blood pressure. Hypotension may therefore be very significant following bolus administration of propofol, particularly in the elderly, medically compromised, and hypovolemic patients. Propofol also leads to dose-dependent respiratory depression and can produce apnea at higher doses. It is not associated with histamine release and has bronchodilatory properties.

Recovery from anesthesia with propofol has several unique characteristics. Compared to other induction agents propofol is associated with a more rapid awakening and recovery, with less residual CNS effects. Many patients also experience mild euphoria on awakening, which enhances reported satisfaction with the anesthesia postoperatively. Even at subhypnotic doses propofol is associated with decreased postoperative nausea and vomiting.9 All these features make propofol an attractive choice for outpatient procedures where decreased time to discharge is desirable. Even with an available generic formulation the higher cost compared to barbiturates is still apparent.

The increased cost can overshadow the advantages of using propofol infusions, especially if the surgical time is long (> 2 h), or if quick discharge is not required. Several considerations should be taken when using propofol. The solution can cause significant pain on injection, especially in smaller vessels. This may be attenuated with pre-administration of opioids or 1% cardiac lidocaine. Unlike barbiturates, however, it does not cause vasospasm when inadvertently injected into an artery. Anaphylaxis is rare but has been reported in patients with a history of allergic reactions to other medications, especially neuromuscular blocking drugs. A history of egg allergy does not necessarily preclude the use of propofol, as the egg protein contained in the suspension is lecithin, whereas most egg allergies consist of a reaction to egg albumin. The original proprietary agent, Diprivan, uses ethylenediaminetetraacetic acid as an antibacterial agent, whereas the generic version contains a sulfite. Although this generic agent should not be used in patients with known sulfite sensitivity, it appears that allergic reactions and bronchospasm are very unlikely, although not completely unheard of, in other patients including asthmatics. Both drug suspensions are pH neutral and can support bacterial growth; therefore, the observation of sterile technique and discarding of an opened vial or filled syringe after 6 hours are recommended. Cracked glass containers or discolored contents should be discarded, as sepsis is a possibility.

 Etomidate Like midazolam, etomidate contains an imidazole structure (Figure 5-7). It is water soluble but available in a 0.2% solution in propylene glycol. In the same way as the other induction medications, etomidate interacts at the GABA receptor. Etomidate is used primarily as an induction agent for general anesthesia at 0.2 to 0.4 mg/kg IV. Its main advantage over barbiturates and propofol is cardiovascular stability. Although systemic blood pressure can decrease by up to 15% with etomidate, changes in heart rate are minimal. It also does not depress myocardial contractility. Etomidate is usually reserved for patients with unstable cardiac disease because it is more expensive than other induction agents. Spontaneous respiration may be maintained.

Respiratory depression is less pronounced with etomidate compared to barbiturates, although apnea is still possible with higher doses. Etomidate is metabolized by both hepatic enzymes and plasma esterases. This rapid clearance leads to awakening and recovery that is faster than with thiopental but slower than with methohexital or propofol. Myoclonus is common in over 50% of patients and may be partially prevented with pre-administration of a benzodiazepine or opioid. Many patients experience pain on injection secondary to the propylene glycol. Etomidate has been associated with adrenocortical suppression but this is less profound when only a single induction dose is administered.

Ketamine Ketamine is a phencyclidine derivative (Figure 5-8) that induces a state of “dissociative anesthesia.” This is characterized as a “dissociation” between the thalamocortical and limbic systems, producing a cataleptic state during which the patient may appear awake but does not respond to commands.11 The eyes may be open and nystagmic. Ketamine does produce anterograde amnesia, and unlike other induction agents, it can produce intense analgesia. Unlike other hypnotic agents ketamine does not interact with GABA receptors. The exact mechanism of action is unclear but ketamine is a nonselective antagonist of supraspinal N-methyl-Daspartate receptors,which involve the excitatory neurotransmitter glutamate. Inhibition of these receptors decreases neuronal signaling and is likely responsible for some analgesic effects. Ketamine may also interact with pain receptors in the spinal cord as well as opioid receptors, which may also account for analgesia.12 Ketamine is highly lipid soluble and redistributes quickly, which accounts forits rapid onset of action and relatively short duration. It is metabolized by hepatic enzymes and has an active metabolite, norketamine.

Ketamine does have a significant abuse potential and chronic use can lead to enzyme induction. The cardiovascular effects of ketamine reflect its indirect activation of the sympathetic nervous system. Ketamine causes an increase iorepinephrine by inhibiting reuptake at postganglionic sympathetic neurons. Sympathetic stimulation increases heart rate and systemic blood pressure. Ketamine should therefore be used with caution in patients with uncontrolled hypertension or in whom tachycardia should be avoided. However, ketamine may be chosen for induction of general anesthesia at 1 to 2 mg/kg IV when cardiovascular stimulatory effects are desired, as in emergent trauma surgery. Practitioners should note that ketamine is actually a direct myocardial depressant, an effect normally masked by the indirect sympathetic stimulation. In severely compromised patients, however, catecholamine stores may be exhausted and hypotension secondary to myocardial depression can become significant. Respiratory depression is not significant with ketamine, although apnea will occur with rapid bolus administration.

Upper airway reflexes remain largely but not reliably intact; aspiration is still possible, especially as ketamine increases salivary secretions and postoperative nausea and vomiting. Ketamine does not cause histamine release and is a potent bronchodilator secondary to sympathetic activation as well as direct bronchial smooth muscle relaxation. In oral surgical practice a primary indication for ketamine is intramuscular injection for uncooperative adult patients, such as the mentally challenged or those with severe psychiatric illness, or for children who will not tolerate IV placement. The intramuscular dose for induction of general anesthesia is 3 to 7 mg/kg, whereas 2 to 3 mg/kg is usually sufficient to obtain adequate control for IV placement. A water-soluble benzodiazepine like midazolam is commonly added to reduce the possibility of uncomfortable dreaming associated with ketamine. An anticholinergic medication like glycopyrrolate is also given to reduce the production of salivary secretions secondary to ketamine. Glycopyrrolate may be preferred over atropine or scopolamine for its superior antisialagogue effects, less pronounced cardiac effects, and poor CNS penetration.

The other main use in oral surgical practice is in an IV deep-sedation technique. Conscious sedation is first achieved with a benzodiazepine, followed by subanesthetic doses of 10 to 30 mg of ketamine until a state that is similar to deep sedation is achieved. Although ketamine is quite analgesic some surgeons also add an opioid in the baseline sedation. Alternatively, if a standard deep-sedation technique with methohexital has been applied (see “Methohexital,” above) and large doses of the barbiturate become necessary to achieve adequate sedation, or unwanted patient movement persists despite high methohexital doses, the addition of small boluses of ketamine can often enhance the quality of sedation. “Emergence delirium” can occur during awakening. The patient may experience visual and auditory hallucinations that can be perceived as either pleasant (euphoria) or unpleasant (dysphoria), lasting for up to several hours. Delirium occurrence is less common in children and with doses less than 2 mg/kg IV. It may be attenuated with prior or concurrent administration of benzodiazepines, which should be routine when intravenous sedation techniques are used. Inhalation Anesthetics Inhalation anesthetics include nitrous oxide (N2O) as well as the potent volatile halogenated agents, such as halothane, isoflurane, sevoflurane, and desflurane.

N2O alone is commonly used in dental offices for anxiolysis and mild sedation, but it is also used in combination with other medications to induce and maintain both sedation and general anesthesia. The halogenated agents are extremely potent and are used for induction and maintenance of general anesthesia. The pharmacokinetics of these anesthetic agents differ from those of intravenous medications. These drugs are inhaled and cross from the alveoli into the pulmonary vasculature, entering the general circulation. They are able to cross the blood-brain barrier and exert anesthetic effects within the brain.

Except for halothane most of these agents are minimally metabolized and are subsequently excreted unchanged back into the alveoli. Once exhaled these gases are deposited into the anesthesia circuit and eventually scavenged. Plasma concentrations of the inhaled anesthetics are dependent on the concentration of the gas within the alveoli, solubility characteristics of the individual gases, and cardiac output.13,14 Cardiac output influences the rate of uptake from the alveoli. Main factors affecting alveolar gas concentration include the inspired concentration of gas, alveolar ventilation, and the total gas flow rate.

Administering a higher concentration of gas will increase intra-alveolar concentration, whereas altering the total gas inflow or alveolarventilation (respiratory rate, tidal volume) will affect how quickly the concentration of gas within the alveoli changes. Each agent varies in its solubility in blood and other tissues such as the brain and fat, and these characteristics determine the ease with which the gas crosses into the different tissues. Of these, the blood:gas solubility coefficient (Table 5-1) is the most useful in describing the onset and offset of action of an anesthetic gas. The blood:gas solubility coefficient expresses the extent to which the anesthetic gas molecules from the alveolar spaces will dissolve into plasma before the plasma solution becomes saturated. Conceptually, a lower coefficient means that the gas is less soluble in blood and will saturate the plasma compartment quickly. Additional “overflow” molecules will then be free to move into other highly vascular tissues such as the brain, where the CNS anesthetic effect takes place. A lower blood:gas coefficient therefore translates into faster onset of action at the brain. Once the gas is discontinued and the alveolar and plasma concentrations decrease, the gas molecules move down their concentration gradient from the tissues back into the blood stream and then into the alveoli. Gases with lower blood:gas coefficients will likewise “offload” from the blood stream into alveoli more quickly and can translate into a faster offset of action. Unlike intravenous medications these inhaled drugs are not administered in doses of mg/kg. The equivalent of the effective dose (ED50) of inhaled anesthetic agent is the minimum alveolar concentration (MAC). The MAC value of any given agent is the inhaled concentration (volume %) of that agent required to prevent movement in 50% of patients to a surgical stimulus. MAC values for different agents are given in Table 5-1.MAC values provide a useful dosage guide for anesthetic gases. In adults a level of 1.3 MAC will prevent movement in 95% of patients, whereas 1.5 MAC (MAC-BAR) will block an adrenergic response in 95% of patients. Below 0.3 MAC (MAC-Awake), patient awareness is more likely. MAC values are additive; for example, if 0.5 MAC of N2O and 1.0 MAC of isoflurane are given simultaneously, the total MAC of anesthetic agent administered to the patient is 1.5 MAC. It should be noted that MAC values are general guidelines, and individual anesthetic requirements can be influenced by a variety of factors such as age or medical status. Neonates have the lowest MAC requirement, whereas children have the highest requirement. MAC requirements subsequently decrease in the elderly patient. MAC values are typically listed for adult (30- to 35-year-old) patients at 1 atm pressure and 20°C. The exact mechanism of action of inhaled anesthetic agents at the CNS is still controversial. Earlier theories have suggested that anesthetic molecules insert into and disrupt the lipid bilayer of neuronal cell membranes, thus interfering with the cellular function. More current theories suggest that anesthetic molecules may instead directly interact with cellular proteins, possibly with membrane ion channels or even specific receptors.

Whereas N2O has mild or minimal sympathomimetic effects, all of the halogenated agents produce generalized cardiovascular depressant effects. The potent volatile agents block peripheral vasoconstriction thus lowering mean arterial blood pressure. At lower doses below 1 MAC the baroreceptor sympathetic reflex is activated, which leads to a compensatory increase in heart rate. The exception is halothane, which in addition to directly depressing myocardial contractility, blocks the baroreceptor reflex. This resulting decrease in cardiac output can lead to a precipitous drop in systemic blood pressure with higher doses of halothane. Halothane also has the highest association with cardiac dysrhythmias. Halothane induction commonly suppresses sinoatrial node activity, leading to the development of junctional rhythms. It also sensitizes the myocardium to catecholamine-relatedventricular dysrhythmias (Figure 5-9), particularly under conditions of hypercarbia. 15 Isoflurane, sevoflurane, and desflurane are not significantly associated with an increased incidence of epinephrineassociated dysrhythmias.

Epinephrine contained in local anesthetic solutions should be limited to a maximum dose of 1 to 2 μg/kg during halothane anesthesia whereas up to 3 to 4.5 μg/kg is considered safe with the other three agents. Under halothane anesthesia, administration of 1.0 to 1.5 mg/kg cardiac lidocaine IV immediately prior to intubation reduces the incidence of ventricular dysrhythmias during this stimulating period when endogenous epinephrine release may occur. Hypoxia and hypercarbia also lower the threshold for dysrhythmias and should be especially avoided with halothane anesthesia. Treatment of the presenting dysrhythmia should be managed as required, including hyperventilation, deepening of anesthetic level and, if indicated, discontinuation of halothane with administration of an alternative anesthetic agent. At usual doses N2O does not appreciably affect respiration. However, the halogenated agents produce a characteristic “rapid and shallow” spontaneous breathing pattern. A decrease in tidal volume is accompanied by an increase in the frequency of breaths, but the faster respiratory rate does not fully compensate for the smaller tidal volumes. Therefore, minute ventilation is reduced and arterial CO2 levels will be elevated in patients spontaneously breathing while under general anesthesia with these agents. The halogenated agents also cause a dosedependent decrease in airway resistance and produce bronchodilation. Hypoxic pulmonary vasoconstriction is attenuated at 0.1 MAC for all volatile agents. Although hepatic blood flow decreases with these agents, hepatic damage, if any, resulting from hypoxia is usually subclinical and transient.Hepatotoxicity is more of a concern with halothane administration. Renal blood flow and urine output are reduced secondary to the decreased mean arterial pressure. The release of fluoride from the halogenated gases does not appear to cause clinically significant damage to renal tissues. With sevoflurane, fresh gas flows should be at least 2 L/min to minimize compound A accumulation in the CO2 absorber which can lead to very rare hepatic or renal damage. Malignant hyperthermia (MH) is another rare but very dangerous reaction triggered by the halogenated agents as well as SCh. N2O, nondepolarizing neuromuscular blockers, opioids, benzodiazepines, and other intravenous anesthetic agents do not trigger MH. Exposure to these medications causes an abnormal receptor in skeletal muscle cells to release excessive intracellular calcium, leading to uncontrolled muscle contractions. As a result CO2 production increases quickly and exhaled CO2 rises sharply. Initial signs include tachycardia and tachypnea, along with muscle stiffness. Metabolic acidosis and hyperkalemia develop next and cardiac arrest is a possibility. Increasing body temperature is a relatively late sign.

The halogenated agent must be discontinued at once and 100% O2 given, preferably through a different circuit and machine. Dantrolene at 2.5 to 10 mg/kg IV must be given as soon as possible. Cooling measures including cooled IV fluids should be instituted. Emergency help must be obtained immediately and the patient will require medical management and monitoring for at least 24 hours following the episode. Reemergence of the reaction is common, requiring re-administration of dantrolene, and acute renal failure is the most common morbidity secondary to myoglobinemia. A mortality rate of 10% is associated with an acute MH episode, even with immediate proper management. Nitrous Oxide N2O is commonly administered in dental offices for anxiolysis and mild sedation. It is a colorless and odorless gas, available in blue cylinders. In the dental setting it is commonly administered with a nasal hood and appropriate scavenger system. Concentration ratios of N2O:O2 range up to 70:30 on most N2O and anesthesia machines.High levels of N2O:O2 alone can produce sedation and significant analgesia. Unexpected respiratory depression or airway obstruction can occur when N2O is added to other sedative agents. N2O in O2 is likely the most commonly used sedative agent in dental offices and enjoys the unique advantage of not requiring an escort after completion of the procedure provided adequate recovery time has elapsed. The drug can be titrated, usually starting at 20% N2O and gradually increasing to 50% as needed. Doses above that level are associated with increased nausea and dysphoria, although the brief application of doses higher than 50% is useful during local anesthetic administration and other short stimulating surgical episodes. At the conclusion of N2O sedation, 3 to 5 minutes of 100% O2 is administered to prevent diffusion hypoxia; if room air O2 is given instead, the rapidly exiting N2O candilute the O2 concentration in the alveoli to hypoxic levels during recovery. With a low blood:gas solubility coefficient of 0.47, N2O has a very quick onset and recovery.While N2O lacks the potency of the halogenated agents at a MAC value of 105, it also lacks the respiratory and cardiovascular side effects. During general anesthesia it is often administered to an intubated patient in combination with other medications such as halogenated gases and opioids. Using this combination can reduce the dose required of each drug if given singly and will lessen the incidence of potential side effects. N2O is also inexpensive and can reduce the total cost of administered drugs.

 There are a few contraindications for the use of N2O. It can enter closed spaces faster thaitrogen can exit, leading to distention of the closed space.13 In oral surgical practice the implication of this property is to avoid N2O use in patients with current otitis media and sinus infections and with emphysema (blebs). Other contraindications of N2O use include current respiratory disease and a history of severe postoperative nausea. Several precautions should be exercised when using N2O. It has been implicated in producing sexual hallucinations in some patients, predominantly young women. An additional person such as an assistant should always be present when this gas is being administered. Patients with preexisting psychiatric disorders may experience exacerbated symptoms while undergoing N2O sedation. Because low levels of N2O in room air have been demonstrated to increase spontaneous abortion rates in pregnant anesthesia providers, proper scavenging is essential to minimize room air levels so that surgical personnel are not at increased risk. Frequent recreational use of N2O has been reported to lead to peripheral neuropathy and other deleterious effects. As with all anesthetic agents anesthesia providers must never use these drugs for personal use and should be alert to potential misuse by other providers of these drugs.  

  Allergy to local anaesthetic agents used in dentistry – what are the signs, symptoms, alternative diagnoses and management options?

Summary  Allergy to amide local anaesthetics is rare. Allergic reactions are most likely to occur with the ester local anaesthetic agents; these are not used routinely in dentistry. Adverse effects experienced after administration of local anaesthetics may be mistaken for allergic reactions, but often there is another explanation for the symptoms.  True allergic reactions to local anaesthetics are either immediate (type I; angioedema, urticaria, pruritus, tightness of the chest, wheezing, fall in blood pressure) or delayed (type IV; localised reaction at the injection site, contact dermatitis) hypersensitivity reactions. Due to the rarity of local anaesthetic allergy, if a patient experiences signs and symptoms suggestive of an allergic response, consideration should be given to other possible causes of the symptoms e.g. toxicity (sedation, light headedness, slurred speech, mood alteration, diplopia, disorientation and muscle twitching) or a psychogenic reaction (anxiety, flushing of the skin, blotchy red rash, bronchospasm, sweating, tachycardia, syncope, hyperventilation, nausea and vomiting). Where local anaesthetic allergy is strongly suspected, patients should be referred for allergy testing for confirmation.

   Background Following the administration of a local anaesthetic, a minority of patients may suffer one of a range of unwanted symptoms. Some of these symptoms can be mistaken for hypersensitivity or allergy and the patient unnecessarily told they are allergic to the anaesthetic. Mislabelling of patients as allergic to local anaesthetics can lead to problems for dental practitioners with patients unable to undergo routine dental treatment [1].  

Local anaesthetic agents can be categorised into two classes: amide (lidocaine, bupivacaine, prilocaine, ropivacaine, articaine, mepivacaine) and ester (benzocaine, cocaine, procaine, tetracaine). True allergy to an amide local anaesthetic is exceedingly rare. Local anaesthetics of the ester type are more likely to produce allergic reactions as they are metabolised to para-aminobenzoic acid (PABA), which is an allergenic compound [2,3,4,5]. The only ester local anaesthetic used in dentistry is benzocaine, which is used in topical preparations applied prior to administration of local anaesthetic injections. An allergy to one ester local anaesthetic contraindicates the use of another ester, as the metabolism of all esters yields PABA. Patients are unlikely to show cross sensitivity to amide local anaesthetics as these are not metabolised to PABA. Allergy to one amide local anaesthetic does not contraindicate use of another amide local anaesthetic [3,6]. However, it would be unwise to use another amide local anaesthetic without hypersensitivity tests [6].   This Q&A addresses the signs and symptoms of local anaesthetic hypersensitivity, differential diagnoses and the management of a patient with suspected allergy to local anaesthetics.   

Answer Local anaesthetics are considered relatively safe, but, given the high number of injections that are administered adverse reactions are inevitable [3]. Adverse systemic reactions to local anaesthetics can be divided into three categories: toxic, psychogenic and allergic [3].   

Signs and symptoms of local anaesthetic hypersensitivity  A true allergy to local anaesthetics may be either type I or type IV [7].  Type I; immediate anaphylactic reactions mediated by IgE antibodies. Signs and symptoms of type I allergy tend to occur within minutes of giving the injection:  The lips and periorbital areas swell (angioedema).  The patient may become agitated and there is generalised urticaria and pruritus, particularly of the hands and feet. Other symptoms include abdominal cramps, nausea and diarrhoea [8].  Tightness of the chest, with wheezing and difficulty in breathing may occur. There may be a fall in blood pressure and a rapid thready pulse, which may be accompanied by flushing of the skin or rash [8].   Type IV; delayed hypersensitivity reactions mediated by sensitised lymphocytes:  Usually localised to the injection site.  Commonly expressed as a contact dermatitis [7].   

Alternative diagnoses Genuine hypersensitivity reactions to local anaesthetics are extremely rare. It has been estimated that true allergic reactions to local anaesthetics account for less than 1% of all adverse reactions to local anaesthetics [1, 7,9]. It is unclear where this figure originates from or the number of patients this represents, as the incidence of adverse reactions occurring in patients who have received local anaesthetics is not reported. Adverse reactions commonly mistaken for hypersensitivity reactions include syncope (fainting), panic attacks and toxic effects due to inadvertent entry of the drug into the circulation [10]. The following are possible differential diagnoses and their symptoms: 

1. Allergy  Many allergic reactions involving local anaesthetic preparations are due to other constituents in the injection solution rather than to the drug itself. Excipients such as preservatives (e.g. benzoates – used in multidose vials) and antioxidants (e.g. metabisulphites – used in local anaesthetic solution containing adrenaline) can cause allergic reactions [4, 11].   Allergy to latex contained in rubber bungs, natural rubber latex gloves, rubber dams and other dental materials should also be considered [4,12].     Historically, the most sensitising components in local anaesthetic solutions were preservatives such as methylparabens. Parabens are no longer added to dental local anaesthetic solutions available in the UK [3,10,13].  

 2. Psychogenic Psychogenic reactions (originating in the mind, an emotional response) are one of the most common adverse reactions associated with local anaesthetic use in dentistry. They may manifest in many ways, the most common being syncope but other symptoms include panic attack, hyperventilation, nausea, vomiting and alterations in heart rate or blood pressure, which may cause pallor. They can be misdiagnosed as allergic reactions and may also mimic them with signs such as flushing of the skin, blotchy red rash, oedema and bronchospasm [3,8].  All patients have some degree of autonomic response to injections, ranging from slight tachycardia and sweating to syncope [14].

  3. Toxic Toxic reactions may occur if high levels of anaesthetic enter the blood stream. Local anaesthetics can reach the systemic circulation as a result of repeated injections, inadvertent intravascular administration or overdose in those patients who have problems eliminating or metabolising the anaesthetic [14, 15]. Toxic side effects are predominantly neurological and include excitability or agitation, sedation, light headedness, slurred speech, mood alteration, diplopia, disorientation and muscle twitching. Higher blood levels may result in tremors, respiratory depression and seizures [3, 15].   Vasoconstrictor agents such as adrenaline may also cause adverse effects. Adrenaline toxicity can result in symptoms such as anxiety, restlessness, trembling, pounding headache, palpitations, sweating, pallor, weakness, dizziness and respiratory distress [6].   Toxic reactions can be minimised by staying within safe dosage parameters and using safe injection techniques [14]. 

  Management options to prevent adverse effects occurring

When a patient experiences signs and symptoms that are suggestive of an allergic reaction, possible alternative causes should be considered such as contact with other common allergens, toxic dose or a psychogenic reaction. The possible causes of the symptoms experienced should be discussed with the patient. Use of the terms ‘allergic’ and ‘allergy’ should be avoided when discussing any adverse event as this term is recognised by patients and readily adopted as the explanation [16].   Adverse reactions caused by toxicity or anxiety can be minimised by [16]:  Administering injections with an aspirating syringe to avoid intravascular injection [10,16].  Relaxing nervous patients to relieve their anxiety. For extremely anxious patients, sedation may be required. Treating patients in a supine position to prevent fainting. Giving injections slowly to reduce discomfort and improve localisation of solution. Restricting the total dose given to the patient to prevent toxic effects occurring by overdose. The maximum dose for the individual patient can be calculated using the dosage information contained in the package insert or recognised dental textbooks on local anaesthesia, and taking into account the age and weight of the patient, any concomitant drug therapy and underlying medical conditions.  

Management of a patient who suffers an adverse reaction in the surgery  Psychogenic reaction: If a fall in blood pressure occurs or the patient feels faint, laying the patient flat and elevating the legs should be sufficient to help restore the blood pressure [17]. Any tight clothing around the neck should be loosened [18]. Once conscious, the patient should be given a glucose drink [17]. Calm the patient and reassure them.  Toxic reaction: Symptoms caused by toxicity will be short lived in most patients. The pharmacokinetics of the local anaesthetic agents used in dentistry suggest that the drug will be eliminated from the blood stream within a couple of hours, but may be as long as 12 hours in some individuals. Reassure the patient that they will feel better after several hours and inform them that although the reaction is unpleasant it should not happen again and it is not necessary to avoid that local anaesthetic in the future.   

Management of a patient when local anaesthetic allergy is strongly suspected If symptoms suggestive of a true allergic reaction occur, (localised reaction consisting of swelling, erythema, an itchy rash or systemic features such as dyspnoea, wheezing, widespread skin rash or circulatory collapse) the patient should be given emergency treatment following the ‘Emergency treatment of anaphylaxis guidelines’ (see ‘Medical emergencies in dental practice’ in the ‘Prescribing in dental practice’ section of the current BNF or http://www.resus.org.uk/pages/MEdental.pdf  for details). If the patient feels unwell, their condition is deteriorating or they are very distressed they should be transferred to hospital [12].   The patient should be referred for further investigation to confirm if the local anaesthetic or another possible allergen (e.g. excipient, latex) was the cause of the adverse effects [16, 17]. If the cause of the symptoms is uncertain, dentists should contact the local dental hospital to discuss referring the patient for further investigation. Alternatively, if a true allergic reaction is suspected, patients can be referred by the dentist or GP directly to the allergy clinic at their local hospital, if this service is available [8]. Location and contact details for allergy clinics can be found via the British Society for Allergy and Clinical Immunology website: http://www.bsaci.org   Very rarely allergy to the local anaesthetic is confirmed. In these cases immunological testing should be extended to other local anaesthetics in order to identify a safe alternative for future dental procedures [9].         

Management of patients who report to be allergic to local anaesthetic agents New patients who claim to have had an allergic reaction to a local anaesthetic should be carefully questioned to obtain a history of past events [5]. These details may be more reliably obtained from the patient’s previous dentist.  Questions to ask the patient or dentist include:  What symptoms did the patient experience?  What explanation for the symptoms was given at the time? Who told them this?  Have they ever had any other dental treatment or surgery in the past that required them to have a local anaesthetic agent – what happened?  Have they any other allergies? Have they ever been tested for a local anaesthetic allergy? If so, what was the result? (The allergy specialist should be contacted for confirmation and further information).    Management:  If further information obtained strongly suggests an allergy but no details are available, refer the patient for allergy testing.  If further information strongly suggests a psychogenic reaction, proceed with care and address the patient’s anxiety.  If further information strongly suggests toxicity, proceed with care starting with low doses of local anaesthetic/vasoconstrictor.  If no information is available from the patient or dentist, contact the GP who may have information about previous local anaesthetic exposure or other relevant knowledge.  If it is strongly suspected that the patient has previously suffered an allergic reaction to a local anaesthetic and emergency dental treatment is required, consider contacting a local hospital dental department to discuss management and referral to a unit that has full resuscitation facilities available.

  Local Anesthetics in Dentistry: Then and Now  Local anesthetics have been in use in dental practice for more than 100 years. The advent of local anesthetics with the development of nerve blockade injection techniques heralded a new era of patient comfort while permitting more extensive and invasive dental procedures. A brief history and summary of the current local anesthetics available in the United States is provided, and some of the newest techniques for delivering local anesthetics are reviewed. General guidelines for addressing difficulties encountered in anesthetizing patients are also discussed. The first local anesthetic agent to be widely used in dentistry was cocaine. Centuries before European exploration of the New World, Peruvian Indians had found that chewing leaves of the coca plant produced exhilaration and relief from fatigue and hunger. Following the import of coca leaves to Europe, much research was conducted to elucidate the properties of the coca leaf extract. In 1859, Albert Niemann refined the coca extract to the pure alkaloid form and named this new drug “cocaine.” Niemann recognized the anesthetic effect of cocaine when he noted that “it benumbs the nerves of the tongue, depriving it of feeling and taste.”1 In the summer of 1884, Carl Koller, a junior resident in the University of Vienna Ophthalmological Clinic, conducted experiments to test the topical anesthetic properties of cocaine on the corneas of various lab animals and on himself (self-administration being common in medical research at that time). He found that the drug rendered the corneas insensitive to pain. In September of that year, Koller performed the world’s first operation using local anesthesia induced by topical cocaine on a patient undergoing glaucoma correction.2 The noted American surgeon William Halsted was the first person to inject cocaine for nerve conduction blockade, performing infraorbital and inferior alveolar nerve blocks for dental procedures in November 1884.3 Halsted subsequently developed numerous other regional nerve block injection techniques, many of which are still fundamental to dental practice. Despite its promise for pain management during surgery, cocaine had major drawbacks, such as a high propensity for addiction and a short duration of action.

The latter factor necessitated injection of large doses of the drug, increasing the potential for severe systemic toxicity. One technique developed to counteract this short duration/high dose problem was to apply a tourniquet near the operative site. In addition to the risk of local tissue damage, this approach had limited success in many regions of the body and was impractical for anesthesia of the oral cavity. In 1903, Heinrich Braun reported that epinephrine could be used as a “chemical tourniquet” when added to a solution of cocaine by producing localized vasoconstriction to slow the rate of vascular uptake, and thus reducing the required dose of cocaine.4 However, the drawbacks of cocaine were still significant, and research to find a synthetic substitute was widely undertaken. In 1905, Alfred Einhorn and his associates in Munich reported their discovery of procaine, an ester-based synthetic local anesthetic.5 Procaine was immediately accepted as a safe substitute for cocaine. Some historians consider the discovery of procaine to mark the beginning of the modern era of regional anesthesia. Several other ester-type local anesthetics were subsequently developed and remained in wide use in the United States throughout most of the 20th century. In 1943, Nils Löfgren, a Swedish chemist, synthesized a new amide-based local anesthetic agent, derived from xylidine, and named it “lidocaine.”6 Lidocaine was more potent and less allergenic than procaine and the other ester-based anesthetics. Since Löfgren’s discovery of lidocaine, several other amide anesthetics have been developed for use in dental procedures: mepivacaine, prilocaine, bupivacaine, etidocaine, and articaine. The advantages of the amide-based anesthetic agents, particularly their very low rate of allergenicity as compared to the ester-type anesthetics, led to their gradual and complete replacement of the ester-based anesthetics in dental use. The last ester anesthetics packaged in a dental syringe cartridge were discontinued in the mid-1990s.  

Current Dental Anesthetic Agents  Today’s availability of a variety of local anesthetic agents enables dentists to select an anesthetic that possesses specific properties such as time of onset and duration, hemostatic control, and degree of cardiac side effects that are appropriate for each individual patient and for each specific dental procedure. Table 1 lists the anesthetic agents available for dental use in the United States and briefly summarizes their properties. It should be noted that these properties, particularly duration and depth of anesthesia, are only approximations and are variable due to a number of factors:7 * Individual variation in response to the drug administered; * Accuracy in administration of the drug; * Status of the tissues at the site of drug deposition (vascularity, pH); * Anatomical variation; and * Type of injection administered (supraperiosteal [“infiltration”] or nerve block). 

Lidocaine  Lidocaine is considered the prototypical amide anesthetic agent. At its introduction in 1948, it was roughly twice as potent and twice as toxic as procaine, producing a greater depth of anesthesia with a longer duration over a larger area than a comparable volume of procaine. Consequently, lidocaine quickly became the most popular local anesthetic in dentistry. It is available in the United States in three formulations: 2 percent without vasoconstrictor (plain), 2 percent with 1:100,000 epinephrine vasoconstrictor, and 2 percent with 1:50,000 epinephrine. Lidocaine without vasoconstrictor has a softtissue anesthetic duration of one to two hours, but a pulpal duration of only five to 10 minutes and is therefore of limited use for most dental procedures. Both formulations with the epinephrine vasoconstrictor have a pulpal duration of one to 1.5 hours and a soft-tissue range of three to five hours. The 1:50,000 epinephrine concentration may be advantageous for hemostasis in surgical sites but has no significant advantage for duration of pulpal anesthesia. Mepivacaine Introduced in 1960, a 2 percent solution of mepivacaine has potency and toxicity ratings roughly equivalent to a 2 percent solution of lidocaine. The greatest advantage of mepivacaine is that it has less vasodilating activity than lidocaine (all anesthetic agents without an added vasoconstrictor are vasodilators to some degree) and can therefore be used reliably as a nonvasoconstrictor-containing solution for procedures of short duration.7 Mepivacaine is available on the U.S. market as either a 3 percent plain solution or a 2 percent solution with 1:20,000 levonordefrin. The plain solution has a pulpal anesthetic duration of 20 to 40 minutes with a soft-tissue duration of two to three hours. The vasoconstrictor-containing solution has a pulpal duration equivalent to that of lidocaine with vasoconstrictor, that is, pulpal anesthesia for one to 1.5 hours and soft-tissue duration of three to five hours. It should be noted that although the levonordefrin vasoconstrictor in mepivacaine is less likely to produce cardiac side effects, such as palpitations, than is epinephrine, it is more likely to increase blood pressure and does have a higher potential for interaction with tricyclic antidepressants such as amitriptyline hydrochloride.8-10 At the time of this writing, levonordefrin production has been discontinued in the United States and existing supplies of mepivacaine with levonordefrin are expected to be exhausted by early to mid-2003. However, a potential new producer of levonordefrin is currently running production tests and may have mepivacaine with levonordefrin back on the U.S. market by mid to late 2003.11   

Prilocaine  Prilocaine, also introduced in 1960, is slightly less potent and considerably less toxic than lidocaine as a local anesthetic agent. Like mepivacaine, prilocaine produces less tissue vasodilation than lidocaine and can be used reliably in plain solution form for short-duration procedures. Prilocaine is available as a 4 percent plain solution or as a 4 percent solution with 1:200,000 epinephrine. The plain solution has a pulpal duration of 40 to 60 minutes with soft-tissue anesthesia for two to three hours. It is worth noting 3that the duration of anesthesia with plain prilocaine is more dependent upon the type of injection given than are other anesthetics. Infiltration injections of prilocaine plain may only provide five to 10 minutes of pulpal anesthesia while regional block injections typically show the commonly described 40- to 60-minute durations. The vasoconstrictor-containing solution provides pulpal anesthesia for one to 1.5 hours like lidocaine and mepivacaine with a potentially longer soft-tissue duration of three to eight hours.7 Anecdotally, prilocaine has been said to have greater efficacy in patients who are difficult to anesthetize, for example, patients with a past or present history of substance abuse. An additional advantage is the decrease in cardiac side effects due to the lower vasoconstrictor concentration. Relative contraindications for the use of prilocaine include a patient history of methemoglobinemia, anemia, or cardiac or respiratory failure due to hypoxia.7 An additional precaution is raised by reports of a significantly increased risk of nerve paresthesia with the use of prilocaine and articaine, particularly for inferior alveolar and lingual nerve block injections.12,13 Haas, the lead author of a number of these studies, has speculated that chemical toxicity may be the cause of these increased paresthesias since the only common feature of prilocaine and articaine is that they are both 4 percent concentration anesthetic agents.14 His hypothesis is supported by reports of neurologic deficits with 4 percent lidocaine in animal studies15 and in human studies using 5 percent lidocaine for spinal anesthesia.16-18 This suggests that reduction of dosage to the absolute minimum amount required for effective anesthesia and the use of a slow, atraumatic injection technique with repeated aspirations are wise precautions if either of these anesthetic agents is selected for use with inferior alveolar and lingual nerve block injection techniques at all. 

Bupivacaine  Bupivacaine is an analogue of mepivacaine that exhibits a fourfold increase in potency and toxicity and a remarkable increase in the duration of anesthesia. Released in the United States in 1983 and available only as a 0.5 percent solution with 1:200,000 epinephrine, bupivacaine may exhibit a slightly slower time of onset in some patients, approximately six to 10 minutes compared with two to seven minutes for lidocaine and mepivacaine.4 The longer duration of anesthesia for which bupivacaine is known is achieved primarily via regional nerve block injection techniques with mandibular blocks frequently having greater duration than maxillary blocks. As a block, pulpal durations of 1.5 to seven hours are common with soft-tissue anesthesia of five to 12 hours. When administered via infiltration technique, bupivacaine provides anesthetic depth and duration comparable to other local anesthetic agents.

Articaine  Articaine is an analogue of prilocaine in which the benzene ring moiety found in all other amide local anesthetics has been replaced with a thiophene ring. Although not released in the United States until April 2000, articaine has been available in Germany since 1976 and in Canada since 1983 in a number of formulations. To date, only one formulation has been approved in the United States, a 4 percent solution with 1:100,000 epinephrine. With a higher per-cartridge unit cost and a pulpal anesthesia duration of approximately one hour with soft-tissue anesthesia for two to four hours, it would initially appear that articaine is a less attractive agent for dental applications. However, with a slightly faster onset of action (1.4 to 3.6 minutes19), reports of a longer and perhaps more profound level of anesthesia,20,21 and most notably frequent practitioner anecdotes of a greater ability to diffuse through tissues, articaine has become a very widely used anesthetic in the European and Canadian markets. The tissue diffusion characteristics of articaine are not well-understood; however, in a variable percentage of patients, a maxillary infiltration injection in the buccal vestibule will result in adequate palatal anesthesia for tooth extraction. Similar results have been claimed for the mandibular anterior and premolar teeth with buccal infiltrations.19 As discussed with prilocaine, reports of a significantly increased risk of nerve paresthesia with the use of articaine and prilocaine, particularly for inferior alveolar and lingual nerve block injections,12,13 warrants practitioner caution in the use of these anesthetic agents.

 The Difficult-to-Anesthetize Patient  Many factors may affect the success of local anesthesia, some within the practitioner’s control and some clearly not. While no single technique will be successful for every patient, guidelines exist that can help reduce the incidence of failure. For this discussion, a failure will be defined as inadequate depth and/or duration of anesthesia to begin or to continue a dental procedure. Due to a number of factors, such as thicker cortical plates; a denser trabecular pattern; larger, more myelin(lipid)-rich nerve bundles; and more variable innervation pathways,22-29 more problems of inadequate anesthesia occur in the mandibulary arch than in the maxillary. Although failures are more common in the mandibular arch, maxillary failures do occur and can be equally frustrating.  The Maxilla  Most problems with maxillary anesthesia can be attributed to individual variances of normal anatomical nerve pathways through the maxillary bone (Table 2).30 While the pulpal sensory fibers of the maxillary teeth are primarily carried in the anterior, middle, and posterior superior alveolar nerves, which also supply the buccal soft tissues, accessory pulpal innervation fibers may be found in the palatal innervation supplied by the nasopalatine and greater palatine nerves.30 By careful application of topical anesthetics, distraction techniques (application of pressure and/or vibration), and slow delivery of the anesthetic agent, palatal injections can be given with very little to no patient discomfort. With the availability of articaine hydrochloride 4 percent with epinephrine in the United States, many practitioners are finding that palatal injections may not be necessary when it is injected into the maxillary buccal vestibule.20 Additionally, new computer-controlled anesthetic delivery systems are particularly adept at eliminating, or at least minimizing, the discomfort of palatal injections.31-33 Such systems are discussed in greater detail under New Delivery Systems and Techniques.  The Mandible  Problems with mandibular anesthesia are most common in the molar region but are by no means limited to these teeth.23-29,34

As in the maxilla, most anesthesia problems encountered in the mandible are due to individual variations in the nerve pathways, in other words, accessory innervation (Table 2).34,35 The first, and simplest, guideline relates to the extent of anesthesia achieved. If, for example, a patient reports profound anesthesia of his or her lower lip and tongue after receiving an inferior alveolar and lingual nerve block injection, but the tooth in question is still sensitive, it is probable that those two nerves have been successfully anesthetized and that the tooth sensitivity is very likely due to accessory innervation. This conclusion is based upoerve morphology. Fibers near the periphery of a nerve bundle tend to innervate the most proximal structures, i.e.,molars in the case of the inferior alveolar nerve; while fibers min the center of the nerve bundle tend to innervate the most distal structures, i.e., the incisors in this example.7 If a patient reports that his or her lower lip and the tip of his or her tongue are anesthetized, structures that are innervated by the most central fibers of the inferior alveolar and lingual nerve bundles respectively, than it seems reasonable to conclude that these two nerves are indeed anesthetized and that accessory innervation to the sensitive tooth likely exists in this patient. For mandibular molars, a common, and therefore important, accessory pathway to be considered is the long buccal nerve.27,36-38 This nerve branches from the anterior division of the mandibular portion of the trigeminal nerve high within the infratemporal fossa and crosses the anterior border of the mandibulary ramus above the retromolar pad to enter and innervate the mucosa and overlying skin of the cheek, including the mandibular buccal attached gingiva.

Due to the possible branching of this nerve as it descends along the medial surface of the mandibular ramus, a high injection site along the long buccal nerve pathway may offer a greater likelihood of successfully anesthetizing more of these accessory branches.26 Such a site for blocking the long buccal nerve is to inject into the soft tissue just medial to the anterior border of the ramus at or above the same level above the mandibular occlusal plane as the inferior alveolar block injection is given, i.e., using the depth of the coronoid notch anteriorly as the landmark for the horizontal level of the injection.4 An added benefit of this site is improved patient comfort by injecting medial to the anterior border of the mandible rather than into 5 the lateral tissue. An additional source of accessory innervation to any mandibular tooth is the mylohyoid nerve.23-25,28,39 This nerve arises from the inferior alveolar nerve at a variable level above the mandibular foramen and may not be consistently anesthetized with a conventional inferior alveolar block injection.40 Although it is anatomically described as a motor nerve innervating both the mylohyoid and the anterior belly of the digastric muscles, the mylohyoid nerve has been clearly shown to carry sensory fibers to mandibulary teeth.28,39 A mylohyoid nerve block may be delivered by injecting into the floor of the mouth between the medial surface of the mandible and the sublingual fold formed by the sublingual salivary gland. The injection should be given just distal to the sensitive tooth, and the depth of the injection should approximate the root apices.41 An alternative technique to anesthetize the mylohyoid nerve is to administer a second inferior alveolar nerve block at a higher and/or deeper site.34

 This may better approximate the origin of the mylohyoid nerve as it branches from the inferior alveolar nerve, but this technique does carry an increased risk of intravascular injection and possible hematoma.35,42 A potentially more efficient method for dealing with accessory innervations in the mandible is to use a more complete mandibular block technique such as the Gow-Gates43 or Vazirani-Akinosi44 techniques (Table 3). These injections, first described in the early 1970s, are given at higher sites on the mandibular ramus (Figure 1) and are aligned relative to the maxillary occlusal plane rather than the mandibular. Properly performed, these techniques have a very high success rate coupled with a very low risk of positive vascular aspiration.45 It should be noted, however, that even a high mandibular division nerve block technique, such as the Gow-Gates, may not have a 100 percent success rate in anesthetizing all possible nerve branches to mandibular tooth pulpal tissues.46,47

or this reason, the best advice is to be proficient with a variety of mandibular injection techniques as described in detail in the dental literature. Another concern is the situation where anesthesia of all apparent nerve pathways is achieved, but the duration is short and/or the depth of anesthesia is poor. Giving a second injection into the same site as the first injection may prove adequate simply due to the increased volume of anesthetic solution. However, using a different anesthetic agent for the second injection may increase the likelihood of successful duration. This difference may be explained by individual variances in tissue pH conditions and differing characteristics of each anesthetic agent, such as dissociation characteristics, lipid solubilities, and receptor site protein-binding affinities. No contraindication exists for using any of the amide anesthetic agents in combination with one another; however, care must be taken to limit the total dosage of anesthetic given to the maximum amount allowable for the agent with the lowest permissible dosage. For all injections given, the precise amount of each agent injected and the specific site of each injection should be recorded in the patient’s treatment record. It is particularly helpful to note if one agent appears to have worked better than another. In these cases, this “better” agent should be used for the first injection at the next appointment. The “Hot” Tooth

Anesthetizing the “hot” tooth, a condition generally indicating an irreversible pulpitis, can be one of the most frustrating problems for any dental practitioner. Whenever possible, prescribing antibiotic therapy to reduce inflammation and allowing the site to settle down may constitute the best course of action. When such a course is not an option, the first step in working through this situation is to deliver an appropriate nerve block injection as far back as possible along the innervation pathway of the hypersensitive tooth. If all of the surrounding soft tissues are numb, but the tooth itself is still sensitive, use of an intraosseous technique, which has a highly predictable success rate, is recommended.48-50 Less predictable, but also potentially effective, is a periodontal ligament injection technique.51-53 A last resort is to quickly access a pulp horn, creating a hole just large enough to insert a needle, and injecting anesthetic directly into the pulp chamber of the tooth. The major limitation of all three of these injection techniques is the inability to anesthetize multiple teeth with a single needle penetration and the relatively short duration of anesthesia achieved.53,54 6 New Delivery Systems and Techniques In the past decade, two delivery systems have been developed that utilize computer technology in the administration of local anesthetics to patients. The Wand (Milestone Scientific) and the Comfort Control Syringe (Dentsply) both recognize that the more slowly an injection is given, the less traumatic it is to the tissues of the injection site and therefore the more comfortable the injection is to the patient. The Wand precisely controls the flow rate and modulates fluid pressure by use of a computer microprocessor and an electronically controlled motor to deliver the anesthetic solution at a slow rate regardless of tissue resistance.55 This allows the operator to deliver the anesthetic solution into any injection site, including the palate, at a rate that is potentially below the threshold of pain. An additional advantage is the smaller diameter of the syringe/handpiece itself, which permits the operator to use a more comfortable and stable pen grip on the syringe, allowing for more natural use of finger rests while injecting. The smaller size of the syringe may also be less intimidating to patients, a significant consideration when working with a dental-phobic patient.33,56-58 Disadvantages of the Wand system include the initial cost of the unit, approximately $1,400; the cost of the disposable syringe/handpiece assembly per patient, approximately $1; the longer/slower injection time; and, due to the volume of the tubing connecting the motor unit to the handpiece, only 1.4 ml of anesthetic solution can actually be delivered from each anesthetic cartridge.57 Additionally, the system does require some time to get accustomed to: The system is operated by a foot-pedal control, and the anesthetic cartridge is not directly visible in the operator’s hand. This latter factor is addressed by a series of audible sounds that inform the operator of how much anesthetic solution has been delivered.Introduction of the Wand delivery system has renewed interest in the palatal approach to anesthesia of the anterior and middle superior alveolar nerves.58,59 Using the palatal approach, anesthesia of the pulpal tissues of the maxillary incisor and premolar teeth, as well as anesthesia of the buccal and palatal gingival tissues, may be accomplished without the side effect of facial anesthesia found with the infraorbital nerve approach. Preservation of normal facial sensation and movement is an advantage for mid-procedure smile line assessment of maxillary anterior cosmetic procedures, and patient acceptance is an additional advantage. On a precautionary note, it is imperative that this injection be administered very slowly with constant visual monitoring by the operator to avoid excessive tissue blanching. The recommended injected volume is 0.6 to 0.9 ml administered over a 60- to 90-second, or longer, interval. If excessive tissue blanching is observed during the injection, a momentary pause to allow return of normal blood supply, indicated by return of pink coloration to the tissue, is recommended. A risk of palatal tissue ulceration must be recognized if marked ischemia occurs.58,59 The Comfort Control Syringe is a newer entry in the electronic, computer-controlled anesthetic delivery system market. This preprogrammed unit controls the delivery rate of anesthetic solution for a selection of injection techniques (block, infiltration, palate, PDL, intraosseous) preselected by the operator. Although bulkier than the Wand syringe/handpiece, the Comfort Control Syringe also enables the operator to use a pen grip while injecting. The Comfort Control Syringe houses the anesthetic cartridge directly behind the needle, just as in a traditional syringe; and the injection controls are fingertip accessible on the syringe rather than via foot pedal. The initial unit cost is approximately $900 with disposable supplies costing approximately 55 cents per patient.58-61

Although the technique of delivering local anesthetics directly into alveolar bone in close proximity to root apices is not new, recent technology has greatly improved the convenience of intraosseous injections. Systems marketed by Stabident, X-tip, and Intraflow have been incorporated into many dental practices. The intraosseous technique is quite reliable for pulpal anesthesia for one or two teeth and is particularly useful for anesthetizing the “hot tooth.” Primary pulpal anesthesia using an intraosseous technique is effective in 45 percent to 93 percent of cases with short duration of approximately 30 minutes.54 When used as a supplement to an inadequate conventional infiltration or nerve block injection, the intraosseous technique is effective in 80 percent to 90 percent of cases with profound anesthesia of moderate duration (60 to 90 minutes).54 7 Intraosseous injections require a system for penetrating the cortical plate of bone so that the anesthetic agent may be injected into the cancellous tissue space from where it then diffuses to the desired root apices. The Stabident System (Fairfax Dental) is a two-part system with a separate perforator needle that mounts to a low-speed handpiece. The anesthetic injectioeedle is then passed through the perforation into the cancellous bone. One cause of difficulty with this system is the necessity of aligning the injectioeedle precisely with the perforation channel to gain access to the cancellous space. This problem has been addressed in the Stabident System by adding a funnel-shaped needle guide that is inserted into the perforation channel. The X-Tip System (X-Tip Technologies) has also addressed this problem in its system design. The X-Tip is also a two-part system, similar to the Stabident, with the exception that removal of the perforator needle leaves a cannular guide for insertion of the anesthetic injectioeedle into the cancellous bone.

The Intraflow System (IntraVantage) is based upon a special low-speed handpiece with a clutch and footpedal control system that permits perforation and injection with the handpiece in place, thus removing the need to switch from handpiece to syringe. The Intraflow handpiece system is about $900; the cost of disposable supplies is similar for all three systems, ranging from $1.50 to $2. Because intraosseous injections are into the highly vascular cancellous bone tissue space, use of vasoconstrictor-containing anesthetic agents is generally not advised due to the rapid uptake of the agent into the circulatory system with a subsequent increase in patient heart rate.49,50, 62-64 In a number of studies, from 2 percent to 15 percent of patients reported moderate to severe pain during perforation, needle insertion, or injection of the anesthetic solution; and equal numbers of patients reported postoperative pain, swelling, or bruising at the injection site.54 A variety of electronic anesthesia systems have come and gone from the dental marketplace. Although these systems had their clinical successes, most practitioners found them frustrating to use in routine practice. The increased time for patient education about use of the system and the large variance in predictable anesthesia from one patient to the next, and even between different sites on the same patient, have ultimately led to their discontinued use. In general, the systems were only useful for relatively noninvasive procedures on a small percentage of patients.  Summary What might be next on the front for dental anesthesia? As dental lasers continue to evolve and become increasingly refined, they may yet reach their early promise of providing “painless dentistry without the needle or the drill.” Such an event will surely usher in a new era of patient comfort, potentially decreasing the number of dental-phobic patients. The prospect is truly exciting.