Chapter 12: Anesthesia

patient? The ASA physical status grade has six classes (1–6) ranging from a normal healthy patient (1) to one that is brain dead (6). The full categories are shown below: Class 1: A normal healthy patient Class 2: Mild systemic disease with no functional limitation Class 3: Severe systemic disease with functional limitation Class 4: Severe systemic disease that is a constant threat to life Class 5: Moribund and not expected to survive without surgery Class 6: Brain dead patient for organ retrieval This has clinical relevance for assessing the risk of surgery for individual patients and can help to guide which procedures can safely be offered and the appropriate level of care a patient will require (e.g., day case versus overnight admission and postoperative ward care versus high dependency). The ASA status also forms part of the World Health Organization (WHO) surgical checklist and facilitates communication between the surgeon and the anesthetist about a patient’s general fitness for surgery. A patient’s ASA status will also impact the billing costs for medical care in most medical systems as well as the clinical outcomes following surgery.1,2

Both induction and maintenance of anesthesia can be achieved with intravenous or inhalational agents. Of all the volatile inhalational agents, sevoflurane is the preferred choice for inhalational induction because it is well tolerated due to its having a low odor and being nonpungent. In contrast, other inhalational agents such as desflurane and isoflurane are extremely pungent and not suitable for induction of anesthesia; they would be likely to cause airway irritation and may cause laryngospasm or bronchospasm if used for that purpose. Nitrous oxide is a gas, which is used as an adjuvant to general anesthesia and as an analgesic during labor and other painful procedures. It can also be used in liquid form for cryotherapy for skin lesions. Entonox is the trade name for a 50:50 mix of oxygen and nitrous oxide which is typically used for analgesia, e.g., dressing changes, labor pains, and in the pre-hospital/emergency room setting. Intravenous induction can be achieved with a number of different substances of which propofol is a very commonly used example. Other agents include etomidate, thiopental, and ketamine.1

Malignant hyperthermia (MH) is a rare and potentially fatal genetic disorder that affects calcium regulation within skeletal muscle. It can be precipitated by a variety of drugs used in anesthesia including succinylcholine and inhalational volatile agents. Succinylcholine is a neuromuscular blocking agent used to induce rapid and profound paralysis, e.g., to facilitate endotracheal intubation and for modification of convulsions after electroconvulsive therapy (ECT). Historically, it was also used to maintain neuromuscular blockade during short procedures. Other potential triggers for malignant hyperthermia include volatile anesthetic agents such as desflurane, isoflurane, and sevoflurane. If given these drugs, people at risk for malignant hyperthermia may develop life-threatening multiorgan failure. Early features of MH include an increase in end-tidal carbon dioxide (even with increasing minute ventilation), tachycardia, tachypnea, muscle rigidity, and hyperkalemia. Later features include fever, myoglobinuria, and multiple organ failure. Patients often have no idea they are susceptible to MH unless they have a first-degree relative who has experienced problems or they themselves have experienced problems previously. There is a muscle biopsy test called the Caffeine Halothane Contracture Test, which can be performed at limited centers throughout the US. However, this is an expensive test to perform costing thousands of dollars. Any concerns raised with respect to MH during preassessment need to be escalated to the anesthetic team for further advice.1–2

Local anesthetic agents work in a broadly similar manner by interfering with sodium channels, thereby preventing an influx of sodium within the neuronal membrane. This does not affect the resting membrane potential but does impair propagation of the action potential. Penetration of the nerve membrane by the local anesthetic agent requires an unionized state (i.e., to be in base form). The pKa determines the ratio of ionized and nonionized local anesthetic and the closer the pKa is to the body pH, the faster the onset of action.1–3 There is a differential sensitivity of nerve fibers that results in smaller fibers and those that are myelinated being blocked more quickly (Fig. 12.1). The clinical sequence is as follows: 1. Vasodilatation 2. Loss of pain and temperature 3. Loss of proprioception 4. Loss of pressure sensation 5. Loss of motor function Fig. 12.1 Sequence of local anesthetic blockade. BLOCK ONSET BLOCK RECOVERY SEQUENCE OF EFFECTS ON FUNCTION • B (Vasodilation) • C, A-δ (Loss of pain/temperature) • A-γ (Loss of proprioception) • A-β (Loss of pressure sensation) • A-α (Loss of motor function)

Local anesthetic agents are classified as either amides or esters depending on their chemical composition. Amides are more commonly used in clinical practice and may be identified by the presence of the letter i in their prefix. For example, lidocaine, bupivacaine, mepivacaine, and prilocaine. The maximum safe dose for lidocaine with epinephrine is 7 mg/kg, but without epinephrine it is only 3–5 mg/kg. Absolute maximum safe dose is 300 mg (not 750 mg). Lidocaine is metabolized in the liver (not the kidney) and its onset of action is rapid (usually within 2 minutes). The elimination half-life is 90–120 minutes and the duration of action is up to 1 hour without and 6 hours with epinephrine. True allergies are rare for amide anesthetic agents such as lidocaine. Paraaminobenzoic acid (PABA) is a by-product of metabolism of esters (such as procaine and tetracaine) not amides and is often responsible for hypersensitivity reactions following administration of these compounds. Methylparaben is a preservative found in some ester and amide local anesthetics that resembles PABA and may cause an allergic reaction.1,2

Lidocaine is a short-acting local anesthetic commonly used in plastic surgery. It is an amide that has a rapid onset of action and is often combined with epinephrine. The safe dose of lidocaine with epinephrine is 7 mg/kg. The safe dose without epinephrine is 3–5 mg/kg. This lady can therefore safely have 38 mL of 1% lidocaine with epinephrine.1–3 The calculation is shown below: 7 mg × 55 kg = 384 mg A 1% solution contains 10 mg in 1 mL Therefore, she can have 384/10 = 38.4 mL Option A is based on a calculation of 2 mg/kg which is a maximum safe dose for levobupivacaine. Option B is based on a calculation of 3 mg/kg which is a maximum safe dose for lidocaine with epinephrine. Option D refers to a safe maximum volume for 2% lidocaine with epinephrine, not 0.5%. Option E refers to a safe volume for 0.5% lidocaine with epinephrine, but would exceed the maximum safe dose for 2% lidocaine with epinephrine by four times. In the clinical setting it is vital to have a good understanding of safe dosing for commonly used local anesthetic agents.1–4

The safe dose of bupivacaine is 2 mg to 2.5 mg per kg and is not significantly altered by the addition of epinephrine.1 This patient can therefore safely have 48 mL of 0.25% bupivacaine or levobupivacaine. The calculation is shown below: 2 mg × 60 kg = 120 mg A 0.25% solution contains 2.5 mg in 1 mL Therefore, she can have 120/2.5 = 48 mL Option A is the maximum safe volume of 1% not 2% bupivacaine. Option B is the maximum safe volume of 1% bupivacaine. Option C is the maximum safe volume of 0.5% bupivacaine. Option E is the maximum safe volume of 0.125% bupivacaine. Levobupivacaine and ropivacaine (Naropin) are both isomers of bupivacaine developed to reduce the cardiotoxicity of bupivacaine. They have become popular alternatives to bupivacaine as a result in many countries. Safe doses are 2–3 mg/kg for levobupivacaine and 3–4 mg/kg for ropivacaine, with maximum recommended doses of 150 and 200 mg, respectively. Use of local anesthetic in patients who have skin grafts taken under general anesthetic is very useful and should be routinely performed. This has the benefit of reducing intraoperative and postoperative pain. Often patients who have split-graft harvest state that the donor site is the most painful part of the procedure so anything that can be performed to minimize this is recommended.1–6

Sodium bicarbonate can be added to local anesthetic solutions to speed the onset of blockade. This works by reducing the acidity of the anesthetic and releasing unionized anesthetic agent. The dose should be 8.4% NaHCO3 added in a ratio of 1:9 with lidocaine. Care should be taken with agents such as bupivacaine as bicarbonate can lead to precipitation. An additional benefit of using bicarbonate is that it can decrease pain during injection, presumably as a result of the decreased acidity and perhaps in part to a more rapid onset of anesthesia.1,2

Using epinephrine with a local anesthetic serves a number of useful purposes but it may increase pain on injection as it requires the solution to be more acidic. This is because epinephrine is unstable in solution at physiological pH.1,2 Other potential disadvantages to utilizing epinephrine include increased myocardial irritability leading to tachycardia, hypertension, or arrhythmias. For this reason, particular caution should be exercised when using epinephrine in patients with cardiac disease. There are multiple beneficial effects of adding epinephrine to a local anesthetic solution. It causes local vasoconstriction and therefore maintains the anesthetic agent at the required site. It reduces bleeding and increases the duration of action. It also enables higher doses to be given safely. For example, lidocaine can be administered at doses of 3–5 mg/kg without epinephrine and up to 7 mg/kg when epinephrine is added. In addition, it will shorten the time to onset of anesthesia. Factors to reduce pain during injection of a local anesthetic include slow infiltration, the addition of bicarbonate, using hyaluronidase,3 and ensuring the product is not cold (particularly relevant in products that are stored in the refrigerator).

Contraindications to using epinephrine in local anesthetics can be classified as absolute or relative. Absolute contraindications include use in the penis, skin flaps with limited perfusion, and when the digital vessels are already compromised. The use of epinephrine in healthy digits is considered safe but dilutions greater than 1:200,000 are recommended. Most of the time a digital tourniquet can be used to reduce bleeding in a digit, negating the need for epinephrine. Relative contraindications for epinephrine use include hypertension, diabetes, cardiac disease, thyrotoxicosis, and certain drug interactions such as with the monoamine oxidase inhibitors (MAO). These can cause a hypertensive crisis when epinephrine is used, secondary to formation of a pool of available endogenous catecholamines.1–4

Bupivacaine is known to have the greatest cardiac toxicity, especially after inadvertent intravascular injection. Levobupivacaine is the L isomer of bupivacaine and was developed to help reduce these cardiotoxic effects. It is often marketed as Chirocaine. An advantage over lidocaine is the prolonged effects of pain relief which can be typically 6–8 hours after injection as a local anesthetic agent. However, the onset of action is delayed compared with lidocaine. Ropivacaine was also developed to provide a long duration of action with less cardiac toxicity and is a popular alternative. Symptoms of cardiovascular toxicity include hypotension, arrhythmias, and cardiovascular collapse. The use of epinephrine can also cause cardiac problems and should be carefully monitored.1–3

Toxicity due to local anesthetics can be unpredictable but generally parallels increasing plasma concentration and tongue numbness and a metallic taste are early signs (Fig. 12.2). Toxicity can be subclassified into central nervous system (CNS), cardiovascular, or idiosyncratic effects. CNS effects include dizziness, metallic taste in the mouth, perioral numbness, tinnitus, and seizures. Cardiovascular effects include hypotension and arrhythmias. Idiosyncratic effects include anaphylaxis in patients with hypersensitivity to esters, increased relative toxicity associated with liver disease and the effects of epinephrine.1–4

Ensuring patient comfort when administering local anesthetic agents is vital and there are a number of key steps that can be taken to minimize patient discomfort during this time. Adding sodium bicarbonate at a ratio of 1:9 parts lidocaine can be helpful in reducing patient discomfort, particularly when the solution contains epinephrine. However, sodium bicarbonate can cause some local anesthetics such as bupivacaine to precipitate, so may be best avoided or used in lower doses such as 0.1–10 mL bupivacaine. In addition, other factors include using a small needle such as 27 or 30 gauge, minimizing number of injection points, administering the agent slowly, using agents without epinephrine where possible (as epinephrine causes the agent to be more acidic), and warming the agent prior to injection. In addition, adding hyaluronidase can reduce pain on local anesthetic administration.1

Mixing of local anesthetics is generally encouraged as there are different benefits involved although the onset, duration, and potency may become less predictable. A mixture of lignocaine and bupivacaine, for example, will combine the benefits of a rapid onset and also a prolonged duration of action. Mixing amides and esters allows for different modes of elimination, which can be potentially helpful. Caution should be exercised when mixing local anesthetics of the same class, e.g., amides, as the documented maximum/toxic doses should be reduced in proportion to the mix. It is vital when doing this to ensure careful calculation of maximum doses by weight. Features of CNS toxicity tend to be dose dependent. Local anesthetics readily cross the blood–brain barrier. Other factors such as acidosis, decreased protein binding, vasoconstriction, and hyperdynamic circulation affect CNS toxicity. Methemoglobinemia is primarily associated with prilocaine use rather than most anesthetics. Liver metabolism of prilocaine forms orthotoluidine which oxidates hemoglobin to methemoglobin. When toxicity is suspected, the initial action should be to stop the injection immediately, then commence supportive/resuscitative care with basic and advanced cardiac life support. Key factors to consider are airway management with high-flow oxygen and management of blood pressure. IV lipid emulsion binds free local anesthetic and should be used in patients with suspected CNS or cardiovascular system (CVS) toxicity. Fig. 12.2 Features of local anesthetic toxicity with increasing plasma concentration. • Cardiac arrest • Respiratory arrest • Convulsions (grand mal seizures) • Muscular twitching/spasms • Tinnitus/auditory hallucinations • Visual disturbance • Disorientation • Light-headedness • Tongue numbness/metallic taste • Antiarrhythmic and anticonvulsant at ≤ �g/ml serum concentration A number of steps can be taken to minimize toxicity, but will not necessarily avoid it. These include using frequent syringe aspirations to reduce intravascular anesthetic delivery, small test doses, and divided dose injection.1–3

A Bier block relies upon intravenous injection of a local anesthetic agent infiltrating the soft tissues of an exsanguinated limb. Due to the cardiac and central nervous system toxicity of local anesthetic agents, the limb must be isolated with a tourniquet and either lidocaine or prilocaine is the preferred agent to minimize risk in the event of unintended systemic spread. A double tourniquet is ideal, allowing greater patient comfort. The proximal tourniquet is inflated first while the block is established. Subsequently the more distal adjacent tourniquet is inflated, which is on tissue which is now insensate, and the proximal tourniquet can be deflated to reduce tourniquet discomfort. A tourniquet must remain inflated for at least 40 minutes to minimize the risk of releasing local anesthetic agent into the systemic circulation. Up to 2 hours of effective block can be achieved.1–3

Spinal and epidural anesthesia have a key role to play in a variety of surgical procedures, particularly of the lower limb and pelvis. Although the two have some similarities, they are quite different procedures with different advantages and disadvantages. Epidural anesthesia involves injection of local anesthetic via a temporary catheter placed in the epidural space. The advantage of this over a spinal injection is that the catheter allows titration of the block as well as later administration of further anesthetic for postoperative pain control. In contrast, a spinal anesthetic involves direct injection of local anesthetic into the cerebrospinal fluid (CSF) at the level of the lumbar vertebrae. Smaller volumes of local anesthetic are required, but it is not possible to increase levels afterwards as no catheter is in situ. A spinal anesthetic typically has a more profound motor block than an epidural which, depending on the site, may have very little motor blockade of the lower limbs. Both types of anesthesia carry risks including hypotension, urinary retention, and headaches. Epidural injections can also be associated with hematoma which, although rare, is important as it must be identified early and evacuated swiftly. Confirmation of diagnosis is usually with magnetic resonance imaging (MRI) scan.1

Routine monitoring of carbon dioxide, although not mandatory during conscious sedation, is highly recommended as it is a reliable indicator for spontaneous airway management and breathing. In addition, other parameters must be regularly assessed including heart rate, respiratory rate, blood pressure, and oxygen saturation. One member of staff needs to be responsible for monitoring the patient while another is performing the treatment. Fasting guidelines for conscious sedation are the same as for general anesthetic. However, surgical management of the airway is not required as the key concept is that the patients are able to maintain their own airway throughout. The rationale for maintenance of starvation times in spite of this is twofold. First, in case there is an airway issue and sufficient loss of consciousness where a risk of aspiration is incurred. Second, in case conversion to a general anesthetic is required due to failure of the procedure to advance without it. ASA status does need to be considered in relation to conscious sedation; however, it is only limited to ASA 1 and 2 patients when performed in the office setting. Clearly conscious sedation does not negate the need for local anesthetic as some form of analgesic is also required.1,2

There are a number of topical local anesthetic agents in common use, the vast majority of which contain lidocaine in varying concentrations between 2.5 and 5%. EMLA contains 2.5% prilocaine and 2.5% lidocaine. EMLA stands for Eutectic Mixture of Local Anesthetic which refers to the situation where two chemical compounds solidify at a lower temperature when mixed together than they do separately. In practical terms, this means that EMLA is a convenient consistency at room temperature for topical use. Key points to remember when using EMLA are that it takes 1 hour to provide an anesthetic effect which then lasts for a further 2 hours, and that it requires placement of an occlusive dressing over the cream once it has been applied. Topical local anesthetics with just lidocaine include LMX-4 and LMX-5 (the number refers to the percentage of lidocaine), betacaine, and topicaine. Tetracaine contains 4% tetracaine only without lidocaine.1–4

It is generally accepted that starvation times for general anesthetic, regional blocks, and conscious sedation are all kept to a 6-hour time free of food and a 2-hour time free of clear fluids. This is to minimize the risk of aspiration during induction of anesthetic, prior to complete airway control. In the emergency setting, a rapid sequence induction of anesthesia can be performed without adherence to these starvation times. In this setting, cricoid pressure is applied by an assistant once the patient is asleep and until full airway control is achieved with endotracheal intubation. In some settings, these starvation times are being reduced. In particular, in pediatric patients, some centers will reduce the clear fluid restriction to minimize the risk of dehydration. The rationale for this is that clear fluids are rapidly absorbed from the stomach and therefore present a low risk of subsequent vomiting and aspiration.1–4