Medical History & Local Anesthesia
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Factors to consider for predicting operative risk include:
- Age.
- Comorbidities.
- Extent and duration of the operative procedure.
- Planned anesthetic techniques.
- The skill set of the surgical team.
- Duration of surgery.
- Available equipment.
- Blood products needed.
- Medications.
- Implants needed.
- Expected postoperative care.
VITALS
Normal body temperature is 98.6 °F or 37°C. Normal heart rate for an adult is 60–80 beats per minute. Normal blood pressure for an adult is approximately 120/80 mm Hg. Normal respiratory rate for an adult is 12–18 breaths per minute.
A complete blood count (CBC) includes:
- Hematocrit/packed cell volume – the percentage volume of red blood cells in whole blood. For males the normal value is 45-50%, for females 40-45%.
- Hemoglobin – the protein inside red blood cells responsible for carrying oxygen. For males the normal value is 14-18g/dL, for females 12-16g/dL. Low hemoglobin levels is termed anemia, increased hemoglobin is called polycythemia.
- Red blood cell count – the number of red blood cells (erythrocytes) per microliter of blood. Normal range for males is 4.7-6.1 million cells per microliter, for females 4.2-5.4 million cells per microliter.
- White blood cell count – the number of white blood cells (leukocytes) per microliter of blood. Normal range for males is 4,500 to 11,000 WBCs per microliter.
- Platelets – Normal range is 140,000-440,000/ml.
ASA PHYSICAL CLASSIFICATION
The American Society of Anesthesiologists (ASA) physical status classification system was developed to give clinicians a simple categorization of a patient’s physiological status to predict operative risk. ASA 1 and ASA 2 need minimal consideration for routine dental treatment. ASA 3 patients exhibit increased risk of a serious medical event. You should consider postponing non-urgent dental treatment until the underlying medical condition can be managed. ASA 4-6 are not generally seen in a common dental setting due to the risk of serious medical complications.
- ASA 1: A normal healthy patient. This patient is not phobic and under 60. No special precautions are necessary.
- ASA 2: A patient with a mild, well controlled systemic disease, with no functional limitations. This can include pregnancy, well-controlled type 2 diabetes, epilepsy, well managed asthma, thyroid dysfunction, treated hypertension, obesity with BMI under 35, frequent social drinker or a cigarette smoker. An ASA 1 patient with significant anxiety or a patient over 60 would be classified as ASA 2. There is still minimal increased risk to operative procedures. Consider treatment modification to help with anxiety.
- ASA 3: A patient with a severe systemic disease that is not life-threatening, but does experience some functional limitation as a result of disease. This includes poorly treated hypertension or diabetes, morbid obesity, chronic renal failure, a bronchospastic disease with intermittent exacerbation (serious asthma), stable angina, myocardial infarction or stroke in the last 6 months, and implanted pacemaker. At rest a patient in the ASA 3 category does not exhibit signs and symptoms of distress, but when stressed (physiologically or psychologically) the patient can exhibit symptoms like undue fatigue, shortness of breath, and chest pain. A patient with angina who is pain free while in the waiting room but develops chest pain when seated in the dental chair is ASA 3. Elective dental treatment is not strictly contraindicated, but the patient should consider postposing non-essential treatment until the patient’s medical status is more stable. Treatment modification is necessary.
- ASA 4: A patient with a severe systemic disease that is a constant threat to life, exhibiting functional limitations from severe, life-threatening disease. This can include unstable angina, poorly controlled COPD, symptomatic chronic heart failure, and a recent (less than three months) myocardial infarction or stroke. The ASA 4 patient exhibits clinical signs and symptoms of disease at rest. Elective treatment should be postponed. In dental emergencies clinicians should treat patients conservatively, preferably noninvasive treatment only (analgesics for pain and antibiotics for infection). More invasive treatment should be performed in an acute care facility (hospital) whenever possible.
- ASA 5: A moribund patient who is not expected to survive without an operation. The patient is not expected to survive beyond the next 24 hours without surgery. Examples include ruptured abdominal aortic aneurysm, massive trauma, and extensive intracranial hemorrhage. ASA 5 patients have more serious problems to worry about. Palliative care only.
- ASA 6: A brain-dead patient whose organs are to be removed
PHYSIOLOGY OF PAIN
Somatic pain is a type of nociceptive pain activated by pain receptors called nociceptors, responding to thermally, mechanically or chemically noxious stimuli. The pain signal travels from the periphery to the spinal cord along A-delta or C fibers. A-delta fibers are thinner and are sheathed in an electrically insulating material (myelin) resulting in its faster signal transduction (5–30 m/s). A-delta pain is quick and sharp.
C fibers are thicker and unmyelinated and signals travel slower (0.5–2 m/s). C fiber pain is slower, duller, often like a burning sensation. These “first order” neurons enter the spinal cord via the Lissauer’s tract, synapsing with second order fibers in the central gelatinous substance of the spinal cord (dorsal horns). The second order fibers ascend in the spinothalamic tract splitting into the lateral (neospinothalamic) tract and the medial (paleospinothalamic) tract, heading to the thalamus.
Visceral pain is similar to somatic pain but mediated by nociceptors in the cardiovascular respiratory, gastrointestinal, and genitourinary systems.
Psychogenic pain (psychalgia) is a pain disorder associated with psychological factors. A person with a psychogenic pain disorder may complain of pain that does not match his/her symptoms. Patients with pain disorders often have comorbid psychiatric disorders, possibly linked to stress, emotional conflicts, psychosocial problems, or various mental disorders.
Neuropathic pain may be associated with abnormal sensations (dysesthesia) or pain from normally non-painful stimuli (allodynia). It may result from disorders of the peripheral or central nervous systems. The prototypical neuropathic pain is trigeminal neuralgia (tic douloureux), usually described by patients as a stabbing, burning or shocking pain that lasts seconds to minutes. Many unlikely stimuli can incite a response including wind, gentle touch, shaving, brushing teeth or thermal stimuli. The cause is not well understood, possibly due to the loss of myelin around the trigeminal nerve.
Trigeminal neuralgia is usually seen in patients over 50 and more common in female patients. One or more of the branches of the trigeminal nerve can be affected, but symptoms do not often cross the midline (unilateral). There is no associated motor function impairment or paresthesia. The main treatment is with the anticonvulsants like carbamazepine (Tegretol), gabapentin (Neuontin), oxcarbazepine (Trileptal) or similar. They may be combined with an antidepressant like amitriptyline (Elavil). Opioids are usually not effective and shouldn’t be prescribed. Surgery (microvascular decompression) can have beneficial effects if the medications don’t work, or side effects are undesirable.
Herpetic neuralgia is a potential result of a herpes zoster (chicken pox) infection. The pain is described by patients as burning, aching, or electric shock. The pain has the potential to be severe. It is treated similar to trigeminal neuralgia, with anticonvulsants, antidepressants, or sympathetic blocks. Ramsay Hunt syndrome is a herpes zoster infection of CN VII and CN VIII resulting in peripheral facial nerve palsy accompanied by a vesicular rash on the ear (zoster oticus) or in the mouth.
Burning mouth syndrome is a painful, complicated condition often described as a burning, scalding, dryness or tingling feeling in the mouth that may occur daily for months. Altered sensation of taste has been documented. It is most often seen in postmenopausal women (5 times more often compared to men). There are no definitive diagnostic tests, no definitive treatment, and the pathophysiology is poorly understood. In half of patients symptoms resolve spontaneously within 2 years.
Many of your patients will suffer from chronic headaches, sub categorized as either:
- Migraines – more common in females, usually unilaterally, severe throbbing pain with photophobia, 1-3 times per month, can last for 4 hours per day for up to 3 days.
- Tension headaches – no sex predilection, usually bilaterally in a band across the forehead, moderate to mild pain described as steady dull ache, intermittent, can last for several hours.
- Cluster headaches – more common in males, unilaterally behind one eye and on the same side each time, excruciating pain, like a hot poker through the eye, 1-3 per day that can last up to 90 minutes, causes eye to water and nose to run.
Temporal arteritis, also called giant cell arteritis (GCA), is an auto-immune condition presenting with persistent headaches. Patients can also complain of mouth related pain in the jaw, tongue, throat and face. Diplopia and ptosis (drooping eyelid) has been documented. It is more commonly seen in patients over 50 years, 2-3 times more likely to be seen in female patients. Microscopic examination shows enlarged cells (giant cell lesions).
Phantom pain sees patients experiencing pain from a non-existent source, a limb or organ, even a tooth.
ANESTHETIC PHARMACOLOGY
An inactive nerve cell has a resting membrane potential of -50 to -70 mV. Excitication leads to the slow phase of depolarization which causes an influx of sodium (Na+) ions through sodium channels along it’s osmotic gradient (higher concentration outside the cell). An increase in positive sodium ions makes the cell transmembrane potential less negative. Once the threshold potential reaches critical level the depolarization causes a flip in polarity, with the inside of the cell more positive compared to the exterior. At the peak of the action potential around +40 mV is reached. This leads to repolarization as potassium (K+) ions pass out of the cell returning the membrane potential to normal. The correct osmotic gradient of potassium and sodium is re-established and maintained by the Na/K ATPase pump.
Local anesthetics reversibly block nerve conduction by blocking cell membrane sodium channels. This prevents the flow of sodium into the cell so the threshold potential is never reached, preventing an action potential. In a myelinated nerve the anesthetic must block a minimum successive number of nodes (of Ranvier) to block the action potential of a nerve (concept of critical length). Potassium, calcium and chloride conductance remains unchanged.
The anesthetic exists in a both ionized and nonionized form when injected. The non-ionized form is able to penetrate the cell sheath and membrane with the help of the lipophilic aromatic ring. Once inside the cell the anesthetic can re-equilibrate between the non-ionized and ionized forms. The ionized form inhibits sodium channels. Small unmyelinated nerve fibers (pain, temperature) and more sensitive to local anesthetic compared to larger, myelinated nerve fibers. This leads to a gradient of effects. Pain fibers are usually affected first, followed by cold, then warmth, touch, deep pressure, and lastly motor fibers. Anesthetic wears off in reverse.
pKa is the negative log of the acid dissociation constant or Ka value. Almost all pKa values of local anesthetics are above 7.4 (physiological pH). The closer the pKa of the anesthetic is to the physiologic pH, the more anesthetic exists in the uncharged base (non-ionized) form which can readily move in and out of cells. So the lower the pKa value, the more rapid the onset (higher proportion of LA is in the soluble form). Infections cause tissues to become acidic, lowering tissue ph from 7.4 to 5-6. This results in a higher concentration of the ionized form of anesthetic leading to poorer penetration through the nerve cell sheath and membrane, decreasing the effectiveness.
FAMILIES OF ANESTHETIC
Lipid solubility affects the LA potency, higher lipid solubility means increased potency. Protein binding affects the duration, the stronger it binds, the longer it takes to wear off. Sodium bicarbonate can be added to increase the pH of local anesthetic, from 3.5 closer to 7, in order to decrease pain when administering, and to increase effectiveness.
All local anesthetics contain an intermediate chain flanked by a lipophilic aromatic ring and an amine group. The ester or amide bond determines the anesthetic classification.
Amides are metabolized by the microsomal P-450 enzymes in the liver via N-dealkylation and hydroxylation. They include Lidocaine (Xylocaine), Prilocaine (Citanest), Mepivacaine (Carbocaine), and Bupivacaine (Marcain).
Esters are metabolized by pseudocholinesterase in the plasma (blood) and include Novocaine, Procaine, Benzocaine, and Tetracaine.
Articaine is unique because it is classified as an amide anesthetic but contains an additional ester group that is metabolized by esterases in blood and tissue. Cocaine is not synthetic and has natural vasoconstrictive properties. Bupivacaine is the longest acting. Topical anesthetic ointments or gels usually contain benzocaine 18-20%.
The addition of a vasoconstrictor like epinephrine decreases the rate of absorption which increases the duration of activity, reduces the rate of systemic toxicity, and helps with hemostasis. Due to its slower clearance the maximum dose for anesthetic containing a vasoconstrictor is larger.
In case of pregnancy, remember the following are considered Class C drugs: bupivacaine, mepivacaine, articaine, epinephrine. It is preferable to use Class B anesthetics: lidocaine and prilocaine.
CALCULATING DOSAGES
Dosage indications are usually based on the “average” 150lb/70kg patient weight. A dentist must be able to calculate safe dosages for patients, in light of their weight and any medical conditions or medications that could affect absorption and breakdown. Remember 1kg = 2.2 pounds. Start by calculating the patient’s weight. Then find the maximum dosage that is allowed to be given to a patient. This will be determined by the manufacturer (of the anesthetic) recommendation, which is usually around 7mg/kg if there is a vasoconstrictor, and around 5mg/kg if there is none. Total maximum dose ranges from 90-600mg depending on the anesthetic used.
100% would be 1000mg/ml or 1g/ml, so 1% Lidocaine means there is 10mg/ml of solution. 2% means there is 20mg/mL of solution. 4% means 40mg/ml. We will use 2% Lidocaine (Xylocaine) as our example. First calculate the maximum dose specific to your patient:
4.4 (mg/kg max) x weight in kg (pounds divided by 2.2). For a 150lb adult this will look like:
4.4 (manufacturer’s recommended maximum) x 68.2 (weight in kg, 150/2.2) = 300mg.
Then calculate how many cartridges you can give so as not to exceed the dose. Cartridges are usually 1.8mL. So for 2% Lidocaine: 20 (mg/ml) x 1.8 (volume of cartridge) = 36 mg/cartridge
300 (max dose) ÷ 36 (dose per cartridge) = 8.3 cartridges for the average patient.
For 2% Lidocaine with 1:100,000 epinephrine the maximum recommended dose would be 7mg/kg. 7mg/kg x 68.2 = 477mg. Each cartridge contains the same amount of anesthetic, 36mg.
477 ÷ 36 = 13.25 cartridges for the average patient.
This maximum number of cartridges is based on the maximum local anesthetic dose, but you may need to be able to calculate the maximum vasoconstrictor dose in case this lowers the numbers of cartridges you can administer. In a healthy person the dose will largely be based on the anesthetic dose, in the case of cardiovascular disease it will depend more on the vasoconstrictor. The vasoconstrictor content is depicted as a ratio and the maximum dose is usually 0.2mg for normal patients and 0.04mg for patients with cardiovascular conditions where a vasoconstrictor could increase the risk of an unwanted cardiac event.
The concentration 1:100,000 means 1g epinephrine in 100,000 ml solvent (ie, 1000 mg/100,000 ml or 1 mg/100 ml). Therefore, 1:100,000 = 0.01 mg/ml and 1:200,000 means 0.005mg/ml (the same vasoconstrictor in double the solution). Each 1.8mL cartridge of 1% lidocaine with 1:100,000 epinephrine contains 0.018mg of epinephrine.
1ml of 2% Lidocaine with epinephrine 1:100,000 will contain the following:
- 20mg of lidocaine – main active ingredient blocking nerve conduction.
- 0.01mg epinephrine – increases duration of anesthetic effect by causing vasoconstriction which decreases absorption. Also helps with hemostasis.
- 6mg of NaCL – establish an isotonic solution.
- 0.5mg sodium bisulfate – antioxidant.
- 1mg methylparaben – bacteriostatic agent, no longer included in single use dental LA cartridges due to potential allergic response.
- Sterile water – provides the volume of the solution in a cartridge.
A 1.8ml cartridge will have above x 1.8.
LOCAL ANESTHESIA TECHNIQUES
All dental and periodontal innervations are from branches of the trigeminal nerve (CN V), V2 the maxillary teeth, and V3 the lower teeth. All dental and periodontal arterial supply is from the maxillary artery, the branch names corresponding to the nerves. All dental and periodontal venous return drains to the pterygoid plexus of veins, which eventually turns into the maxillary vein.
The lower molars (all the lower teeth) are innervated by the inferior alveolar nerve. Anesthesia can be attained by an inferior alveolar nerve block, infiltration into the mandibular foramen area, or local infiltration with an anesthetic with good bone penetration (Articaine). For an inferior alveolar nerve block the anesthetic syringe should bisect the deciduous lower molars/lower premolars on the opposing side.
The point of insertion lies between the coronoid notch (depression on the anterior border of the body of the mandible) and the pterygomandibular raphe (tendinous band that connects the superior pharyngeal constrictor and buccinator) with the buccinator being pierced. The height of insertion is determined by the coronoid notch, in line with the occlusal plane. Deposition of LA at first entry or with withdrawal should accomplish a lingual nerve block. Carefully insert until you hit bone, withdraw 1mm, aspirate, inject ¾ cartridge over 2 minutes (slowly), withdraw 10-15mm, aspirate, slowly inject the lingual nerve, remove.
A long buccal nerve block is required if buccal soft tissue anesthesia is required next to the first, second and third molars. The lingual nerve innervates lingual mucoperiosteum and gingiva adjacent to mandibular teeth. It is often anesthetized during an inferior alveolar nerve block. In lower anterior teeth there can be innervation from the opposite side (nerve anastomosis), so for teeth close to the midline infiltration in this area is advisable.
Maxillary teeth are innervated by the branches of the superior alveolar nerve (posterior, middle, anterior). Local supraperiostial infiltration is effective for most procedures. The middle superior alveolar nerve often innervates the MB root of the maxillary first molar (DB and P root from the posterior superior alveolar nerve). A posterior superior alveolar (PSA) nerve block is available, providing anesthesia for the first, second and third molars (but perhaps not MB root of the first molar). Palatal soft tissue is innervated by the anterior palatine and nasopalatine nerves. An infiltration is usually only required for extractions, not routine restorative work. A block (and infiltration) in the palate is quite painful.
The greater palatine foramen is located halfway between the gingival margin and the midline of the palate, 5mm anterior to the vibrating line (junction of hard and soft palate). It should cause unilateral palatal soft tissue anesthesia up to the first premolar. A nasopalatine block will anesthetize the palate bilaterally, canine to canine. An infraorbital nerve block (anterior superior alveolar) will anesthetize from the midline of the maxilla to the mesiobuccal aspect of the maxillary first molar, affecting the middle superior alveolar, inferior palpebral, lateral nasal, and superior labial nerves (not palatal tissue). Anesthetic is deposited on the inferior margin of the orbital rim at the infraorbital notch, needle penetration over the maxillary first premolar. It is important to apply pressure for 2 minutes after the injection.
A mental block aims to place LA buccal to the apex of the lower premolars, which would anesthetize to the midline. You may find nerve anastomosis means adequate anesthesia is not accomplished for the center teeth.
Needles are selected based on length and outside diameter (gauge). Short needles average 20mm, long average 32mm. A 30-gauge needle averages 0.3mm diameter, 27-gauge 0.4mm, 25-gauge 0.5mm. The smaller the number the larger the diameter. The smaller the diameter, the more difficult it is to perform a reliable aspiration test before injecting, and the more it deflects during placement. Larger needles also break less often, but cause more tissue trauma.
Gow gates technique targets the inferior alveolar, lingual, auriculotemporal, mylohyoid and long buccal nerve. Used as an alternative to the standard inferior alveolar nerve block. It is a true block.
Vazirani-Akinosi technique targets the inferior alveolar, lingual and long buccal nerve, used for uncooperative children or patients with severe trismus. There are no bony landmarks (done “blindly”).
COMPLICATIONS OF LOCAL ANESTHESIA
The maximum dose of anesthetic should not be exceeded to avoid toxicity. An overdose can cause central nervous system (CNS) and cardiac depression, and even death. Toxicity is the most common after accidental intravascular injection or using amounts in excess of recommended maximum dosages. Very young and very old patients are the most at risk of toxicity. Patients may initially experience circumoral paresthesia, followed by initial cardiovascular and central nervous system signs, including:
- Metallic taste.
- Tachycardia.
- Tinnitus.
- Confusion.
- Hypertension.
- Drowsiness.
Later stages of anesthetic toxicity can include
- Hallucinations.
- Bradycardia.
- Hypotension.
- Decreased cardiac output.
- Tremors that can lead to seizures.
- Loss of consciousness.
- Cardiac dysrhythmias.
- Respiratory and circulatory failure.
Allergic reactions to anesthetics are extremely rare but possible. Ester anesthetics are more likely to cause allergic reactions than amides. If a reaction occurs it may be due to the addition of a preservative like methylparaben. Excessive doses of Benzocaine, Prilocaine or Lidocaine can cause the transformation of hemoglobin to methemoglobin which can no longer bind and carry oxygen, leading to a condition called methemoglobinemia. This may present as decreased pulse oximetry and visible cyanosis. Methemoglobinemia is treated with IV methylene blue, 1-2mg/kg of 1% solution over 5 minutes.
