Current Problems in
Surgery ~ Volume 37
Number 1 January 2000
Local Anesthesia in Surgical Practice William P. Schecter, MD Professor of Clinical Surgery University of California, San Francisco San Francisco General Hospital San Francisco, California
Jeffrey L. Swisher, MD Assistant Clinical Professor of Anesthesia University of California, San Francisco San Francisco General Hospital San Francisco, California
I~Vr Mosby
Current Problems in
Sur Volume 37
ry
Number 1
January 2000
Local Anesthesia inSurgical Practice II
Foreword
5
In Brief
6
Biographic Information
9
Introduction
10
Regional Anesthesia in Current Clinical Practice
12
The Anatomy of Peripheral Nerves
12
Physiologic Features of Nerve Conduction
15
The Pharmacologic Features of Local Anesthetics
15 15 17 17 17 20 20 22 22 23 23 23
Structure and Physical-Chemical Properties Metabolism of Ester-linked Local Anesthetics Potency Duration Onset of Action Adverse Reactions Cardiotoxicity Central Nervous System Toxicity Intraneural Injection Methemoglobinemia Allergic Reactions
Principles of Clinical Practice Patient Preparation Balanced Anesthesia Operating Room Environment Medication Accuracy and Sterile Technique Reduction of Drug Injection Pain Curr Probl Surg, January 2000
24 24 24 25 25 25 3
Pre-emptive Analgesia and Local Anesthesia
26
Local Anesthesia and the Management of Chronic Pain
27 28 30
Options for Local Anesthetic Blockade Tumescent Technique for Local Anesthesia for Large Volume Liposuction
Upper Extremity Neural Blockade
30 31 31 33 34
Intravenous Regional Anesthesia (Bier Block) Digital Nerve Block Median Nerve Block Ulnar Nerve Block
Peripheral Nerve Stimulation as an Aid to Peripheral Nerve and Nerve Plexus Block Axillary Block Transarterial Technique Supraclavicular Block Interscalene Block Stellate Ganglion Block Lower Extremity Neural Blockade Lumbar Plexus Anatomy Lumbar Plexus Blockade Blockade of Nerves Arising from the Lumbar Plexus
Sciatic Nerve Block Distal Lower Extremity Block Popliteal Block of the Sciatic Nerve Saphenous Nerve Block Ankle Block Intercostal Block Neuraxial Anesthesia Spinal Anesthesia Epidural Anesthesia
References
4
35 35 36 37 39 40 42 42 44 45 47 48 48 49 49 51 53 53 57 61
Curr Probl Surg, January 2000
.ll,
Foreword Since its first use in a patient who was undergoing a surgical procedure in 1884, local anesthesia, increasingly, has become an integral part of surgical practice and today plays a major role in patient care. With the increased emphasis on outpatient operative procedures and same-day surgery, surgeons are using local anesthetic agents with increasing frequency, and it is imperative that they understand the biochemical and physiologic characteristics of these powerful drugs, the indications for their use, and the potential complications occasionally associated with their administration. In this issue of Current Problems in Surgery, Drs William Schecter and Jeffrey Swisher from the Departments of Surgery and Anesthesia at the University of California, San Francisco, address the topic of "Local Anesthesia in Surgical Practice." Dr Schecter is particularly well suited to author the monograph, having completed residencies in both anesthesia and surgery. Dr Swisher completed a residency in anesthesia and is currently Director of Acute Pain Management at San Francisco General Hospital. They have written an excellent monograph that will appeal to clinicians in all branches of medicine.
Samuel A. Wells, Jr, MD Editor in Chief
Curr Probl Surg, January 2000
5
In Brief Local anesthesia has assumed an increasingly important role in surgical practice because of an improved understanding of perioperative pain management and the increased number of outpatient surgical procedures. Although the leaves of the shrub Erythroxylon coca had been used by the indigenous peoples of South America for centuries, the primary alkaloid cocaine was purified only in 1860 and first used for topical ophthalmic anesthesia by Carl Koller in 1884. Koller's discovery stimulated William S. Halsted, Augustus Bier, and others to extend the use of cocaine local anesthesia to other anatomic areas. By the early twentieth century, infiltration field block, peripheral nerve block, axillary brachial plexus block, intravenous regional anesthesia, and spinal anesthesia had all been described. More extensive use of local anesthesia at this time was limited by cocaine toxicity, leading to a search for the ideal nontoxic local anesthetic that continues to this day. Local anesthetics act by blocking electrical conduction in peripheral nerves. Peripheral nerves are tubular structures that contain millions of axons bundled into fascicles, which in aggregate comprise an individual nerve. Each axon is composed of a phospholipid bilayer cell membrane, which is impermeable to sodium in the resting state. Sodium is therefore the major extracellular cation, and potassium is the major intracellular cation, accounting for the electric gradient from inside to outside the cell o f - 7 0 to -90 mV. The passage of the sodium ion across the cell membrane is limited to 3dimensional protein sodium transport channels, which are concentrated at myelin junctions (nodes of Ranvier) in A-alpha, A-beta, and A-delta peripheral nerves and distributed evenly in nonmyelinated C neural fibers. The local anesthetic molecule binds to protein receptors in the transport channel, thereby preventing sodium influx, cell membrane depolarization, and propagation of electrical nerve conduction. Local anesthetic drugs are tertiary amines containing a lipophilic aromatic ring and a hydrophilic amino group linked by either an ester or an amide. These tertiary amines are weak bases with pKas (25~ ranging from 7.6 to 8.9. Ester-linked local anesthetics such as cocaine, procaine, tetracaine, and chloroprocalne are easily hydrolyzed and are unstable in solution. Esterlinked local anesthetics in vivo are hydrolyzed by the enzyme plasma cholinesterase, one factor accounting for their relatively short duration of 6
Curr Probl Surg, January 2000
action. The metabolic product of ester-linked local anesthetic hydrolysis is para-amino benzoic acid, a chemical found in many cosmetics, skin creams, and some tan oils. Most allergic reactions to ester-linked local anesthetics probably result from previous exposure to para-amino benzoic acid. In contrast, amide-linked local anesthetics are more stable in solution. Allergic reactions to amide-linked local anesthetics are rare. Local anesthetics can be compared by studying their potency, duration of action, time of onset, and toxicity. The in vitro potency of a local anesthetic is related directly to its lipid solubility as measured by the oil/water partition coefficient. The higher the oil/water partition coefficient, the more lipid soluble the drug and the more molecules available to bind with the receptors in the sodium transport channel as the drug diffuses across the lipoprotein cell membrane. Unfortunately, in vivo, higher lipid solubility may also cause redistribution of the drug to fat stores, decreasing its potency. The duration of action of a local anesthetic is a function of the degree of protein binding of the drug. The higher the degree of protein binding, the greater the affinity of the drug for the protein receptor in the transport channel and the longer the drug remains bound to the receptor. Clinically, the duration of the block can be extended by adding epinephrine 1:200,000 to the local anesthetic solution to cause vasoconstriction and delay drug washout. The speed of the onset of drug action is related to the pKa of the drug. The higher the pKa, the more likely the drug is to accept a hydrogen ion and become ionized at a pH of 7.4. The ionized form of the drug will diffuse more slowly across the cell membrane and therefore the onset of action will be slower. The time of onset of the drug can be shortened by increasing the concentration of the drug. The higher the concentration, the more molecules available for diffusion and protein receptor binding and the faster the onset of drug action. Local anesthetic toxicity occurs in 6 ways: cardiac arrhythmias, hypotension, direct tissue toxicity, central nervous system toxicity, methemoglobinemia, and allergic reactions. Systemic toxic reactions are directly related to the concentration of the drug in the blood. The addition of vasoconstrictors to the local anesthetic solution can both decrease the peak blood level and slow the time to peak drug level, thereby permitting safe injection of a larger dose of local anesthetic. Epinephrine should never be used for digital, ankle, or penile nerve blocks because of the risk of gangrene. Although all local anesthetics have potentially negative effects on cardiac function, bupivacaine is the most potent with respect to cardiac toxCurr Probl Surg, January 2000
7
icity. Myocardial depression and cardiac arrhythmias caused by bupivacaine cardiotoxicity are difficult to treat. The development of L-isomers of ropivacaine and bupivacaine may decrease the cardiotoxicity of these drugs in the future. Symptoms of central nervous system toxicity include confusion, hyperactivity, dizziness, tinnitus, seizures, coma, and respiratory arrest. Preliminary needle aspiration and injection of test doses of local anesthetics are advisable to avoid intravascular injection and decrease the risk of cardiac and central nervous system toxicity. Methemoglobinemia is a potentially fatal side effect Of local anesthetics, particularly prilocaine. Prilocaine oxidizes the iron in hemoglobin from the ferrous to the ferric form, resulting in increased affinity for oxygen and tissue hypoxia. The treatment of choice is supplemental oxygen and methylene blue (1-2 mg/kg intravenously). Balanced anesthesia refers to the method of using separate specific drugs to achieve analgesia, amnesia, and muscle relaxation. The development of modern short-acting sedative hypnotic drugs as part of a balanced anesthetic technique has extended the use of local anesthetics to many emotionally labile patients who previously would have been poor candidates. These patients must receive supplemental oxygen and vigilant monitoring during the procedure with electrocardiography, sphygmomanometry, and pulse oximetry. Pain on injection.of the local anesthesia can be reduced by the use of a 25- or 27-gauge needle, injecting slowly and buffering the acid pH of the local anesthetic drug vehicle with bicarbonate. Local anesthetic blocks used before the operation may pre-empt postoperative pain. Although there are sound physiologic arguments that support the concept of pre-emptive analgesia, clinical studies have not yet confirmed the validity of this concept.
8
Curr Probl Surg, January 2000
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William P. Schecter, MD, is Professor of Clinical Surgery and Vice-Chairman of Surgery at the University of California, San Francisco, and Chief of Surgery at the San Francisco General Hospital. After a rotating internship at San Francisco General Hospital, Dr Schecter completed a residency in anesthesiology at the Massachusetts General Hospital and a residency in surgery at the University of California, San Francisco. His clinical interests include trauma surgery and the broad field of general surgery.
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Jeffrey L. Swisher, MD, attended Stanford University for both his undergraduate and medical degrees. He trained in anesthesia , at the Virginia Mason Medical Center, in Seattle, Washington, an institution with a long history of excellence in the field of regional anesthesia. He joined the anesthesia faculty of the University of California, San Francisco, in 1994 after spending a year as a Pain Research Fellow there. He is currently Assistant Clinical Professor of Anesthesia and Director of Acute Pain Management at San Francisco General Hospital.
Curr Probl Surg, January2000
9
,ll
Local Anesthesia in Surgical Practice he introduction of local anesthetics to modern clinical practice occurred during the period of "surgical enlightenment" at the end of the 19th century. However, the bright green leaves of the shrub Erythroxylon coca had been used and even revered by the natives of South America for thousands of years. Coca leaves were used for a variety of medicinal purposes after their importation to Europe in the 16th century. In 1855, Gardeke isolated an active alkaloid from the plant, and he named it erythroxylon. 1 In 1860 Niemann 2 purified and classified the primary active alkaloid, cocaine. Although many chemists and physiologists observed the "numbing" effects of cocaine on the mucous membranes after its purification, 25 years were to elapse before Koller 3 first used cocaine as a surgical anesthetic in 1884. Koller was a 23-year-old house officer at the Allgemeine Krankenhaus affiliated with the University of Vienna. Koller's friend and contemporary, Sigmund Freud, was pursuing his interests in the physiologic and psychologic effects of cocaine. Freud had a compelling personal reason for continuing his research; a close personal friend, Dr von Fleischl-Marxow, became addicted to morphine after its use to control the pain of a thenar stump neuroma, von Fleischl-Marxow had required a thumb amputation to treat a severely infected scalpel wound. Freud had used cocaine injections to treat von Marxow's morphine addiction, resulting in an even worse addiction to cocaine. Freud redoubled his efforts to understand the pharmacologic properties of cocaine and enlisted several of his friends, including Koller, to participate in experiments with the drug. 3 Koller, who was planning a career in the emerging specialty of ophthalmology, was searching for a drug to replace ether as a topical anesthetic for eye surgery. When a friend remarked to Koller that a small sample of cocaine numbed his tongue, Koller immediately realized its potential use as local anesthetic for eye surgery. After a series of animal experiments and the introduction of a solution of cocaine into his own eye, Koller prepared a paper for presentation at the Heidelberg Ophthalmologic Association, which was presented on September 15, 1884, by Koller's friend, Dr Joseph Brettauer, because Koller could not afford to attend the conference. 4 A visiting American surgeon, Dr Henry Noyes, attended the conference and a demonstration of the effects of topical cocaine. He later reported that 10
Curr Probl Surg, January 2000
" . . . the momentous value of the discovery seems likely to be in eye practice of more significance than has been the discovery of anesthesia by chloroform or e t h e r . . . ?,5 Koller's discovery influenced William S. Halsted 6'7 to study the use of cocaine for peripheral nerve blockade. Halsted described both field blocks and peripheral nerve blocks. His successful demonstration of infraorbital and alveolar nerve blockade heralded the widespread use of local anesthesia in dentistry. He was the first to use cocaine for brachial plexus blockade. Unfortunately, Halsted, his associate, Hall, and 3 medical students working with them became addicted to cocaine during the course of their experiments. Halsted and Hall survived their addiction, but the 3 students did not. Coming attempted to apply cocaine to the substance of the spinal cord by intervertebral injection to treat a variety of nervous afflictions. In his second paper in 1885, 8 he described what was undoubtedly central neuraxial blockade in both a dog and a young man. In 1899, Bier9 of Germany, using the aspiration of cerebrospinal fluid (CSF) as an end point, injected cocaine into the subarachnoid space to achieve spinal anesthesia. The use of infiltration and spinal anesthesia spread rapidly, but the high incidence of systemic complications and local tissue ischemia prompted a search for safer local anesthetics similar in structure to cocaine but lacking its toxicity. Procaine was synthesized in the first decade of the 20th century and used by Bier as an intravenous regional anesthetic between 2 Esmarch's tourniquets, l~ A modification of the Bier block is still used today, but only a proximal tourniquet is used. Dibucaine was synthesized in 1928, 4 and tetracaine was synthesized in 1930. 4 Tetracaine remains in use as a long-acting drug for spinal and topical eye anesthesia, but it is too toxic in large doses for infiltration and regional anesthesia. In 1943, Lofgren and Lundquist synthesized the first of a new class of local anesthetic drugs, lidocaine. 4 The center of research and development moved from Germany to Sweden, and many new compounds were synthesized. Mepivacaine was synthesized by Ekstram and Egner in 1956, bupivacaine by Ekstram in 1957, and prilocaine by Lofgren in 1959. Bupivacaine is the most commonly used long-acting local anesthetic in surgical practice today. Although it has a good safety profile, bupivacaine's potential for life-threatening cardiac arrhythmias prompted the pursuit of even safer long-acting local anesthetic drugs. Etidocaine was introduced in 1971 by Tasman but is rarely used because it produces a longer motor than sensory blockade and has significant cardiac toxicity at high blood levels. 4 Curr Probl Surg, January 2000
11
More recently, the L-isomers of the long-acting local anesthetic drugs were discovered to have less cardiac toxicity and equal e f f i c a c y . 11 Ropivacaine was introduced clinically as a pure L-racemate in 1986.12 Lbupivacaine is being launched as an alternative to ropivacaine and the racemate mixture of bupivacaine.
Regional Anesthesia in Current Clinical Practice A recent survey found that, although 97.8% of anesthesiologists in the United States use some regional anesthetic techniques in their practice, relatively few use peripheral nerve blocks. 13 Among these anesthesiologists, 59.7% performed fewer than 5 nerve blocks per month, and lower extremity blocks (femoral [32%], sciatic [22%], popliteal [11%]) were performed less frequently than upper extremity blocks (axillary [88%], interscalene [61%]; P < .001).13 More than 80% of the anesthesiologists 9 surveyed used intravenous regional anesthesia in their practice. The relatively infrequent use of lower extremity blocks is probably due to inadequate training in the specific blocks and the use of peripheral nerve stimulation as an aid to regional block. In addition, the pressures of rapid room turnover and surgeon preference may discourage the use of these blocks. However, lower extremity peripheral nerve blocks are not associated with backache, headache, and postural hypotension that occasionally result from neuraxial techniques to anesthetize the lower extremities.
The Anatomy of Peripheral Nerves Peripheral nerves are tubular structures that contain millions of axons bundled into fascicles, which in turn are bundled into nerves (Fig 1). Each axon is composed of a phospholipid bilayer cell membrane and an internal ion-rich axoplasm, with potassium as the predominant cation. Sodium is the predominant extracellular cation. The passage of sodium across the cell membrane is limited to specific intramembrane transport channels, creating an electric gradient from inside to outside the cell o f - 7 0 to - 9 0 mV. 14 The 3-dimensional protein sodium transport channels are intercalated throughout the phospholipid bilayer (Fig 2). Peripheral nerve axons can be classified according to whether they are covered by myelin. Myelin is a lipid-rich plasma-membrane substance that is manufactured by a special class of Schwann cells and that wraps around the axons of the large sensory and motor nerves (A-alpha, Beta, and A-delta; Fig 3). Functionally, myelin increases nerve conduction velocity by acting as an insulator that shields large portions of the axon from the extracellular sodium-rich environment. 15The sodium channels in 12
Curr Probl Surg, January 2000
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FIG 1. Diagram of a peripheral nerve. (From Strichartz GR.'Neurophysiology and local anesthetic action. In: Cousins MJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: JB Lippincolt Company; 1988. p 25-45. By permission.)
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,, Inlegl-i Prole4n Inlegr~ Perl~',eraJI:~o~ FIG 2. Axonal membrane. (From Strichartz GR. Neurophysiology and local anesthetic action. In: Cousins MJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: JB Lippincott Company; 1988. p 28. By permission.) Curr Probl Surg, January 2000
13
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the axon membrane are therefore clustered at the nodes of the Ranvier between the segments shielded by the myelin. The structure is analogous to a string of beads in which the string covered by the bead is shielded from the environment and the spaces between the beads are open to the environment, allowing ionic flow. Ionic current is limited to the nodal areas, allowing faster "saltatory" or jumping conduction. The nonmyelinated axons (eg, autonomic post ganglionic C fibers) are covered only by a Schwann cell sheath and have the sodium channels distributed uniformly throughout the cell membrane. Each axon is enveloped by an endoneurial connective tissue coating, and each fascicle is enveloped by perineurium. Finally, each nerve is surrounded by epineurium. Functionally, these multiple wrapping layers of 14
Curr Probl Surg, January 2000
/
linkage
R
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FIG 4. Structure of tertiary amine local anesthetic.
connective tissue represent a protective barrier for the nerve and a barrier to the diffusion of local anesthetics (Fig 1).
Physiologic Features of Nerve Conduction The voltage difference of 60 to 90 mV across the resting cell membrane is due to the impermeability of the nerve to sodium flux and the relatively free flow of potassium ions as described by the Nernst equation. ~6 At rest, the electrical potential (-90 mV) is potassium dependent, because of the membrane potassium permeability. During depolarization, the protein channels become permeable to sodium ions. As the sodium ions enter the cell, the transmembrane potential becomes more positively charged, opening the electrically sensitive gates and allowing the inrush of sodium ions. The point at which this in-rush becomes self-sustaining is called the threshold potential. Current flux below the threshold potential will not result in a propagation of the electrical impulse, whereas current flow above the threshold potential results in rapid depolarization of the cell membrane and creation of an action potential to 60 inV. Reaching the threshold potential is an "all or none" phenomenon, much like pulling the trigger of a gun.~7 Hodgkin and Huxley ~4 were the first to demonstrate that the sodium channels are voltage gated and exist in 3 forms: closed, open, and inactivated. The permeability of the sodium channels is a function of the change in 3-dimensional protein conformation. Once the action potential fires, the membrane is in an inactive state before regeneration of the negative membrane-resting potential by energy-dependent active extrusion of sodium across the membrane by the sodium/potassium pump.
The Pharmacologic Features of Local Anesthetics
Structure and Physical-Chemical Properties Clinically useful local anesthetics are tertiary amines containing a lipophilic aromatic ring and a hydrophilic amino group linked together by a chemical bridge (Fig 4). The linkage is either an ester or an amide (Fig 5). Curr Probl Surg, January 2000
15
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These tertiary amines are weak bases with pKas (25~ ranging from 7.6 to 8.9. The lipid soluble local anesthetics act by diffusing across the lipoprotein cell membrane and binding to protein receptors in the sodium channel of the cell membrane, thereby inhibiting electric conduction along the membrane. 18
16
Curr Probl Surg, January 2000
Metabolism of Ester-linkedLocal Anesthetics Ester-linked local anesthetics such as cocaine, procaine, tetracaine, and chloroprocaine are easily hydrolyzed and are unstable in solution. These drugs are hydrolyzed in vivo by the enzyme plasma cholinesterase, which is 1 factor accounting for their relatively short duration of action. 19 The metabolic product of ester-linked local anesthetic hydrolysis is para-amino benzoic acid (PABA), a chemical found in many cosmetics, suntan lotions, and skin care products (Fig 6). The previous exposure of many patients to PABA is the reason why ester-linked local anesthetics have a relatively high rate of allergic reactions compared with amide-linked local anesthetics, z~ Local anesthetic drugs can be compared by studying their potency, duration of action, time of onset, and toxicity (Tables 1 and 2).
Potency The in vitro potency of a local anesthetic is related directly to its lipid solubility as measured by the oil/water partition coefficient. 2~ The higher the partition coefficient, the more lipid soluble the drug and the more molecules available to bind with the receptors in the sodium channel as the drug diffuses across the lipoprotein cell membrane. Unfortunately, the in vivo potency is also affected by the degree of vasodilation (causing washout of the drug) and the redistribution of the drug in adipose tissue. Therefore the clinical potency of the drug cannot be predicted solely on the basis of its lipid solubility. For example, etidocaine is highly lipid soluble and has a greater in vitro potency than bupivacaine but is less potent in vivo. 2~The higher lipid solubility of etidocaine results in greater uptake by the drug in adipose tissue; therefore fewer molecules per milligram drug dose are available for receptor binding when used clinically.
Duration The duration of action of a local anesthetic is a function of the degree of protein binding of the drug. 2~ The higher the degree of protein binding, the greater the affinity of the drug for the protein receptor in the sodium channel, and the longer the drug remains bound to the receptor. The degree of binding to receptor membrane proteins is inferred by measurement of the plasma protein binding of the local anesthetics. 2~The relationship between protein binding and duration of action has been confirmed in vitro 22 and in vivo. 23 The long duration of blockade of bupivacaine and ropivacaine (up to 10 hours after brachial plexus block) 24 is due to their higher protein binding. Clinically, the duration of the block can be extended by adding epinephrine to the solution to cause local vasoconstriction, thereby delaying washout of the drug. Curr Probl Surg, January 2000
17
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TABLE 3. Recommendedmaximumlocal anestheticinfiltration doses
Local anesthetic Procaine Prilocaine Lidocaine Lidocaine with epinephrine 1:200,000 Mepivacaine Mepivacaine with epinephrine 1:200,000 Tetracaine Bupivacaine
Dose by body weight (mg/kg) 14 10 4.5 7 4.5 7 1-2 1-2
Onset of Action The speed of onset of the block in vitro is a function of the pKa of the drug: pKa = pH + log [cation/free base]. Therefore the pKa is that pH at which there are an equal number of ionized and nonionized molecules. Bupivacaine, for example, has a pKa of 8.1. If injected into tissues with a pH of 7.4 (relatively acid), the amino group will tend to accept a hydrogen ion, thereby ionizing the molecule and making it more difficult to diffuse across the cell membrane. 21 In fact, only 15% of bupivacaine exists in the nonionized form at a pH of 7.4 compared with 35% of lidocaine (pKa = 7.7) in the nonionized form, explaining the slower onset of blockade with bupivacaine compared with lidocaine. 21 Clinically, the time of onset of blockade can be affected significantly by the concentration of the drug injected. 2~The higher the concentration, the more molecules available for diffusion across the membrane. The 2 other factors affecting the time of onset of the block are the ability of the drug to diffuse through the tissues to reach the peripheral nerves and the degree of vasodilation caused by the drug. Most local anesthetics induce a biphasic vascular response. At very low doses, they stimulate smooth muscle contraction, thereby causing vasoconstriction. However, at clinically useful doses, all local anesthetics induce vasodilation except cocaine and ropivacaine. The vasodilation can cause wash out of the drug, delaying the time of onset of the block.
Adverse Reactions Adverse reactions to local anesthetics occur in 6 ways: cardiac arrhythmias, hypotension, direct tissue toxicity, central nervous system toxicity, methemoglobinemia, and allergic reactions. Systemic toxic reactions are related directly to the concentration of the drug in the blood. The maximum safe doses of commonly used local anesthetics are listed in Table 3. The site 20
Curr Probl Surg, January 2000
] SAB
FS
BP
E
C
I
FIG 7. Local anesthesia: blood levels and regional anesthetic technique. SAB, Subarachnoid block; FS, femoral/sciatic block; BP, brachial plexus; E, epidural; C, caudal; I, intercostal.
of injection and the volume and concentration of the drug can affect the blood level. The more vascular the site of infection, the greater the uptake of the drug and the more rapid the onset of toxicity. Intercostal injections are associated with the highest blood levels, and subarachnoid injections are associated with the lowest blood levels. The relative effect of the site of injection on the blood level of the drug is illustrated in Fig 7. The addition of vasoconstrictors (eg, epinephrine, ephedrine, phenylephrine) to the local anesthetic can decrease the peak blood level and slow the time to peak blood level by reducing systemic uptake of the drugY The use of vasoconstrictors will therefore permit the safe injection of a larger dose of local anesthetic as a peripheral nerve block. However, the risk of toxic side effects of vasoconstriction such as hypertension, tachycardia, cardiac arrhythmias, myocardial ischemia, and digital gangrene (when injected in the vicinity of the digital arteries) must be considered. 26 When epinephrine is used as a vasoconstrictor, there is no reason to use a concentration higher than 1:200,000 because a higher concentration does not improve the clinical efficacy, yet the risk of cardiac toxicity is significantly higher. 27 Local anesthetics containing epinephrine should never be used for digital, ankle, or penile nerve blocks because of the risk of gangrene. Two other factors affect drug toxicity: lipid solubility and protein binding. The greater the lipid solubility (oil/water partition coefficient), the more rapid the onset of toxicity. The greater the protein binding of the drug, the shorter the time period between the onset of the first symptoms of the central nervous system toxicity and major toxicity. ~9 Curr Probl Surg, January 2000
21.
Cardiotoxicity All local anesthetics have potentially negative effects on cardiac function. Hemodynamic instability may result from hypotension because of smooth muscle relaxation, direct myocardial depression, and cardiac arrhythmias. All local anesthetics with the exception of cocaine and ropivacaine cause vasodilation in the clinical dose range, z~ Ropivacaine in small doses has mild vasoconstrictive properties; at large doses ropivacaine is a vasodilator, z8 The risk of both myocardial depression and cardiac arrhythmia is increased in the presence of hypoxia, hypercarbia, acidosis, hyponatremia, hyperkalemia, and hypotension. 29 Bupivacaine is the most potent local anesthetic with respect to cardiac toxicity. 3~ An inadvertent intravascular injection can produce myocardial depression and cardiac arrhythmia, which are difficult to treat. At blood levels greater than 0.2 gg/mL, a large percentage of the cardiac sodium channel becomes blocked during the action potential, resulting in a "fast-in-slow-out" movement of the drug. In contrast, lidocaine at toxic levels of 10 gg/mL results in only a small degree of cardiac sodium channel block during the action potential. 3~ The depression in conduction caused by bupivacaine results in re-entrant arrhythmias, which can degenerate into ventricular fibrillation. 32 At plasma levels less than 1.5 gg/mL, bupivacaine behaves as a class I antiarrhythmic drug with prolongation of conduction in the His-Purkinje system and the ventricles. At levels greater than 1.5 gg/mL, bupivacaine behaves as both a class I and a class IV antiarrhythmic with depression of both the sinoatrial and atrioventricular nodes and the His-Purkinje and ventricular conduction systems. 32
Central Nervous System Toxicity All local anesthetics have central nervous system side effects, including confusion, hyperactivity, and seizures. The risk of central nervous system toxicity is related directly to the blood level of the drug. Strict attention to proper drug dosage and avoidance of intravascular injection during the conduct of the anesthetic will prevent central nervous system toxicity. The symptoms of mild central nervous system toxicity are lightheadedness, dizziness, tinnitus, and disorientation. Severe symptoms include muscle twitching, tremors, unconsciousness, seizures, and respiratory arrest. 33 All local anesthetics at very high concentrations are cytotoxic to nerve cells, but these concentrations are well above the range of concentrations in clinical use. Permanent neurologic deficits after spinal anesthesia with chloroprocaine were discovered to be caused by bisulfite, a preservative 22
Curr Probl Surg, January 2000
in the drug vehicle, and low pH. Removal of the bisulfite from the solution resolved the problem. 34
Intraneural Injection Intraneural injection of local anesthetics can result in severe nerve injury by 2 mechanisms. The increased hydrostatic pressure within the epineurium can create a compartment syndrome that results in axenolysis and axenotemesis. Furthermore, the needle itself can directly cause injury to nerve fascicles. "A needle is a knife" is a basic clinical axiom. Local anesthetics should never be injected intentionally directly into peripheral nerves. When a peripheral nerve or plexus block is performed, a small test dose should be administered. If the patient experiences severe pain or paresthesia during the test injection, the position of the needle should be adjusted to avoid intraneural injection. 35
Methemoglobinemia Methemoglobinemia is a potentially fatal toxic side effect of local anesthetics. Prilocaine is particularly prone to cause methemoglobinemia. Methemoglobinemia occurs when prilocaine, a secondary amine, oxidizes the iron in hemoglobin from the ferrous to the ferric form, resulting in increased affinity for oxygen and decreased delivery of oxygen to the tissues. The patient experiences the development of clinical signs of hypoxia, including tachypnea, cyanosis, and a fall in the percent saturation of hemoglobin as measured by pulse oximetry. 36 Supplemental oxygen does not result in a significant improvement in the oxygen saturation. Awareness of this clinical syndrome will lead to the correct diagnosis. The treatment of choice is intravenous methylene blue administered in a dose of 1 to 2 mg/kg.37 Methylene blue reduces the ferric iron to ferrous form, thereby restoring oxygen delivery to the tissues. The dose of local anesthetic administered is difficult to control or measure when it is used as a topical oropharyngeal anesthetic, increasing the risk of methemoglobinemia. 36 Methemoglobinemia has also been reported with the use of eutectic mixture of local anesthetic (EMLA) cream, a mixture of prilocaine and lidocaine, in infants and young children to achieve topical cutaneous anesthesia. 38
Allergic Reactions Immunologic reactions to local anesthetics are uncommon. Allergic reaction to ester-linked local anesthetics is more common because of their metabolism to PABA. Allergic reactions to amide-linked local anesthetics are rare. 39 However, compounds such as methylparaben and metabisulfite Curr Probl Surg, January 2000
23
used as preservatives in the manufacture of these drugs can be metabolized to PABA. If an allergic reaction to local anesthetics does occur, skin testing of local anesthetics, methylparaben, and metabisulfite should be performed to identify the precise allergen. 4~
Principles of Clinical Practice Anesthesia has 3 basic components: analgesia, amnesia, and muscle relaxation. Local anesthetics provide analgesia and in some cases muscle relaxation (eg, spinal, epidural, and extremity block anesthesia). They do not provide amnesia or sedation in nontoxic doses. A successful local or regional anesthetic is a partnership between the surgeon, the patient, and the anesthetist. The partnership is based on mutual trust and begins with the preoperative preparation of the patient.
Patient Preparation The preoperative interview is a most important part of the process. A careful and supportive explanation of the details of the anesthetic is actually more important than pharmacologic premedication in achieving a calm state before the operation. 41 The interview is also useful for identifying the occasional emotionally labile patient who is not a candidate for a given procedure with local anesthesia. The degree of emotional lability, the language skills of the patient and the surgical team, and the extent and difficulty of the proposed surgery should be considered in reaching a decision regarding local anesthesia. The introduction of effective short-acting sedatives has extended the indications of local anesthesia to some patients who previously would have been poor candidates. The use of conscious sedation is an important supplement to local anesthesia in many patients. The goal of conscious sedation is achievement of a sedated, amnesic, yet cooperative state without fear or anxiety. There are a wide variety of drugs available, including phenothiazines, butyrophenones, barbiturate and nonbarbiturate hypnotics, benzodiazepines, and ketamine. 42 An in-depth discussion of the pharmacologic properties of these drugs is beyond the scope of this monograph. Modem short-acting benzodiazepines, particularly midazolam, are the most commonly used drugs for both premedication and conscious sedation.
Balanced Anesthesia The short-acting sedative hypnotic, propofol, administered as an intravenous infusion controlled by either the anesthetist43 or the patient, 44 is an excellent drug for achieving "balanced anesthesia." Balanced anesthesia refers to the method of using separate specific drugs to achieve analgesia (ie, 24
Curr Probl Surg, January 2000
a local anesthetic, opiate, nonsteroidal anti-inflammatory drug [NSAID], or some combination thereof), amnesia (eg, midazolam, propofol), and muscle relaxation if necessary. 45 Patients who receive balanced anesthesia require careful monitoring with continuous echocardiography, blood pressure, and pulse oximetry. Supplemental oxygen should be administered. Sedatives should be titrated carefully to avoid the potential complications of respiratory depression and hypotension. Equipment for airway management, cardiopulmonary resuscitation, and administration of general anesthesia should always be immediately available. 46,47
Operating Room Environment The operating room environment can either reduce or augment anxiety. The ambient temperature should be comfortable, and the patient should be kept warm to prevent shivering. Extraneous noise from intercoms, monitor alarms, and inappropriately loud conversation should be kept to an absolute minimum. 48 Intraoperative music chosen by the patient may reduce anxiety, but this effect has not been proved definitively.49,5~Some anesthetists object to music in the operating room because of the potential for impaired vigilance. 5~ Music does not adversely affect the psychomotor performance of anesthetic trainees under laboratory conditions. 52 Patients may listen to music through stereo headsets during surgery without disturbing the surgical and anesthetic teams.
Medication Accuracyand Sterile Technique A regional anesthetic block is a surgical procedure and must be performed with strict sterile technique. Sharp needles should be discarded in impermeable containers immediately after use to prevent occupational transmission of blood-borne infection because of needle-stick injuries. Medication vials should be checked for accuracy before use to prevent inadvertent administration of the wrong drug. Local anesthetics used for digital, ankle, and penile blocks should not contain epinephrine because of the risk of ischemia.
Reduction of Drug Injection Pain Reducing pain during local anesthetic injection can positively affect the course of the entire anesthetic. Four variables affect the amount of pain caused by the injection: (1) the size of the needle, (2) the rate of injection, (3) the pH of the drug, and (4) the anatomic location of the injection. A 25- or 27-gauge needle should be used for cutaneous infiltration. Rapid local anesthetic administration is more painful than slow injection, 53 although this clinical axiom has been challenged recently, s4 Curr Probl Surg, January 2000
25
TABLE 4. Buffer local anestheticsto reduce pain on injection
Local anesthetic LidocaJne/rnepivacaine Bupivacaine/ropivacaine
Volume of local anesthetic
Volume of 8.4% NaHCO s
10 mL 10 mL
1 mL 0.1 mL
Local anesthetics are manufactured in a drug vehicle with a relatively low pH to prevent hydrolysis and extend the shelf life of the drug. The acid medium causes local pain on injection. The pain of local anesthetic injection can be reduced significantly by buffering the drug with N a H C O 3 before injection. 55-58 Lidocaine can be buffered by adding 1 mL of 8.4% NaHCO 3 to every 10 mL of lidocaine. Bupivacalne can be buffered by adding 0.1 mL of 8.4% NaHCO 3 to every 10 mL of bupivacalne (Table 4). We generally do not buffer bupivacaine in our practice because we have not noticed the same degree of pain with injection of bupivacaine that is present with lidocaine. Premedication with an opiate may also have an important role in reducing pain and allaying anxiety during local anesthetic injection.
Pre-emptive Analgesia and Local Anesthesia In a prescient paper, published in 1910, Crile 59 coined the term anociassociation to describe the prevention of "surgical shock" by cocaine blockade of the nerve pathways between the brain and the operative field. Crile reasoned that in the absence of hemorrhage or adverse reactions to inhalation anesthesia, a combination of "applied psychology," morphine, inhalation anesthesia, and local anesthesia would exclude fear, pain, and shock and prevent "exhaustion" of brain nerve cells. In recent years, the spinal cord has become the focus of investigation into the surgical stress response. 6~ The goal of local anesthetic blockade is to prevent sensitization of the spinal cord, which results in persistent hyperalgesia. The molecular basis of this response remains obscure. However, the discovery of a variety of neuropeptides such as substance P, bradykinin, and somatostatin, which function as both neuromediators and intercell chemical messengers involved in the cytokine cascade, has raised the question of a link between the nociceptive and inflammatory responses to s t r e s s . 63-65 The hypothesis that pre-emptive analgesia leads to reduced postoperative pain has not been confirmed definitively in clinical studies to date. 66 Possible explanations for the variable results of the clinical trials to date include (1) inadequate extent of neural blockade, (2) inadequate duration of neural blockade, (3) variable use of narcotics in the control and preemptive groups, (4) variable use of NSAIDs, and (5) surgical procedures that produce minimal pain. 67 26
Curr Probl Surg, January 2000
Until the results of well-designed large multicenter, randomized, prospective trials that evaluate the clinical efficacy of pre-emptive analgesia are available, the use of pre-emptive analgesic techniques is reasonable on the basis of the available data. We recommend careful local anesthetic blockade combined with opioid analgesia, sedation, and NSAIDs (ibuprofen, 800 mg) as a pre-emptive analgesic regimen. 68 This pre-emptive analgesic technique may be used even when general anesthesia is planned.
Local Anesthesia and the Management of Chronic Pain The neurobiologic 69 and pharmacologic 7~ features of chronic pain are complex subjects beyond the scope of this monograph. Local anesthesia, however, plays a limited role in both the diagnostic evaluation and the treatment of patients in chronic pain. Pain has been defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage "m Pain may be classified as transient, acute, or chronic. Transient pain is caused by the activation of nociceptive transducers with actual tissue damage (eg, pinching). Acute pain occurs after activation of nociceptive transducers in an area of local tissue damage (eg, trauma, surgery). Chronic pain is usually caused by an injury or disease but "may be perpetuated by factors other than the cause of the pain "'72 Chronic pain may be further classified as the result of benign or malignant causes. Local anesthetic diagnostic blocks may have a role in the evaluation of selected patients with chronic back pain, myofascial pain, 73 sacroiliac joint syndrome, TM peripheral nerve entrapment, 75 herpes zoster, and reflex sympathetic dystrophy. Patients with pain related to malignancy have a series of graded treatment options available beginning with NSAIDs, acetaminophen, aspirin, and other nonopiate analgesics. For more severe pain, codeine, hydrocodone, or oxycodone may be added to the regimen. For unresponsive pain, morphine, dihydromorphone, or fentanyl patches can be used. A smaller group of patients may benefit from opiates administered through a subcutaneously implanted pump with an indwelling catheter in the epidural space. 76 A very small group of selected patients with localized peripheral neuralgia or visceral pain because of malignancy may benefit from regional block with neurolytic drugs such as phenol and alcohol. A pretherapeutic block with a local anesthetic is important to assess the effect of neurolysis before an irreversible situation occurs. Confirmation of needle placement by computed tomography scan or nerve stimulation is particularly important for cervical and celiac plexus block because of the risk of intrathecal injection. 77 Curr Probl Surg, January 2000
27
Options for Local Anesthetic Blockade Local anesthetic drugs can be used clinically in the following ways: topical spray, topical drops, topical cream, infiltration field block, intravenous regional block, infiltration peripheral nerve or nerve plexus block, epidural block, or spinal block. The choice of drug and technique depends on the planned procedure and the experience and skill of both the anesthetist and surgeon. Topical Spray. Topical sprays are most Often used to anesthetize the oropharynx and trachea for a variety of endoscopic procedures. Viscous lidocaine (Xylocaine) may also be used as an adjunct. Regulation of the precise dose of drug is difficult. Strict attention to the drug dose will help prevent complications such as disorientation, seizures, and cardiac arrhythmias. The association of some topical spray local anesthetics (eg, benzocaine) with methemoglobinemia should be kept in mind. Early recognition and prompt treatment of methemoglobinemia with methylene blue will prevent serious complications resulting from tissue hypoxia. Topical liquid local anesthetics are used to anesthetize the conjunctival sac for many ophthalmologic procedures. Topical Cream. EMLA cream is a topical cutaneous local anesthetic cream that can anesthetize the skin without the discomfort of a needle stick. EMLA cream 5% is a eutectic mixture of the local anesthetics lidocaine and prilocaine. EMLA has found its widest use in pediatric practice and prevents or reduces pain from venipuncture 78 and circumcision. 79 The onset of action after the application of the cream is between 5 and 10 minutes in 83% of patients. 8~ Although the methemoglobin level is elevated to nontoxic levels after EMLA use in neonates (because of prilocaine), 81 a 1-hour application of 1 g of EMLA on intact skin appears to be safe in term neonates under 3 months of age. 82 Infiltration Field Block. The term infiltration field block refers to injection of a local anesthetic drug into and around the skin and soft tissues before surgical stimulation. Smallcutaneous nerves and subdermal nerve endings are blocked with this technique. Most field blocks are easily learned but often have the disadvantage of requiring multiple needle sticks. In addition, the size of the field-block anatomic area may be limited by concerns about local anesthetic toxicity. Field blocks are used routinely to repair cutaneous lacerations and perform a variety of cutaneous and subcutaneous operations including breast biopsy, "lump and bump" surgery, and liposuction. Some commonly performed field blocks require special skill and are described below in greater detail. 28
Curr Probl Surg, January 2000
Field Block for Inguinal Herniorrhaphy. Outpatient inguinal herniorrhaphy with local anesthetic infiltration field block is a standard procedure. The use of supplemental short-acting sedatives such as midazolam (Versed) and propofol has extended the field-block technique to many patients previously considered poor candidates for inguinal herniorrhaphy under local anesthesia. The inguinal region is supplied by cutaneous branches of the T-11 and T-12 intercostal nerves and by the ilioinguinal and iliohypogastric nerves. We use bupivacaine 0.25% as our primary local anesthetic and occasionally add lidocaine 1% (buffered with N a n C O 3 to reduce pain on injection) to speed the onset of the block. The use of lidocaine is not necessary if the field block is injected before formal preparation and draping of the patient. We have not found it necessary to use epinephrine in our local anesthetic solutions to prolong the duration of the anesthetic. The details of the inguinal field block have been organized into separate technical steps83: 1. Subdermal infiltration with 5 to 10 mL of anesthetic solution; 2. Intradermal injection along the intended line of incision; 3. Deep subcutaneous injection of 10 to 20 mL of local anesthetic (at this point we prefer to proceed with the initial incision down to the aponeurosis of the external oblique muscle); 4. Subfascial injection deep to the aponeurosis of the external oblique muscle, with 5 to 10 mL of local anesthetic solution (it is important to inject the drug before the incision of the external oblique aponeurosis; the solution not only anesthetizes the inguinal canal but also lifts the external oblique aponeurosis off of the ilioinguinal nerve, making injury to the nerve less likely); 5. Injection in the area of the pubic tubercle (the injection of several milliliters of local anesthetic into and just superficial to the pubic tubercle blocks this sensitive area, which is not otherwise anesthetized by the field block; the injected solution aids in the dissection and mobilization of the spermatic cord from the pubic tubercle); and 6. Local anesthetic injection into the spermatic cord (this injection aids in the atraumatic dissection of the cord, identification of the hernia sac, and separation of the cord structures from the hernia sac). Spermatic Cord Block. Many scrotal operations such as vasectomy and hydrocoeclectomy can be performed with spermatic cord block. The spermatic cord is gently grasped between the thumb and the index finger just distal to the external ring. One milliliter of 5% Xylocaine is injected with a 25- or 27-gauge needle into the spermatic cord. This will provide excellent anesthesia for the cord and the testicle. Alternatively, larger volumes Curr Probl Surg, January 2000
29
of a lower concentration of Xylocaine (0.5%-1%) can be injected. 84 Additional local anesthetic infiltration of the scrotal skin will permit skin incision and subcutaneous dissection.
Tumescent Technique for Local Anesthesia for Large Volume Liposuction Almost 300,000 liposuction procedures were performed in 1996, and most of the procedures were performed with the tumescent technique for local anesthesia. 85 The tumescent technique involves the segmental injection of warm normal saline solutions Containing dilute concentrations of lidocaine (0.05% to 0.1%), epinephrine (0.5-1:1"100,000), and NaHCO 3 (2.5-12.5 mEq/L). 86 The ratio of fluid injected to ,r of fat aspirated varies from 3:1 to 1.5:1 or less. 87 The estimated safe dose of lidocaine with the tumescent technique has ranged from 35 to 55 mg/kg. 88,89 These doses are far in excess of the manufacturer's recommendation (4.5 mg/kg without epinephrine and 7 mg/kg with epinephrine). In a recent study of the tumescent technique, the peak level of serum lidocaine occurred 12 hours after injection, well after the termination of the procedure. 9~ The number of deaths and complications related to lidocaine toxicity associated with tumescent technique liposuction is unknown because reporting is not mandatory.91Although several careful reports attest to its safety, 88,90 several anecdotal reports in both the lay press and the medical literature allude to deaths that resulted from tumescent liposuction, which may in part be due to lidocaine cardiotoxicity.91 The early signs of lidocaine toxicity (eg, somnolence, dizziness, confusion, slurred speech) may be masked by sedatives commonly used with the "balanced" technique. Caution must be exercised in injecting such large doses of local anesthetics in patients who are taking medications that may aggravate lidocaine cardiotoxicity (eg, beta blockers, monoamine oxidase inhibitors, antidepressants). Further studies are required to determine the true incidence of death related to tumescent liposuction and its relationship to lidocaine toxicity.
Upper Extremity Neural Blockade The options for upper extremity local anesthetic include field block, intravenous regional anesthesia, isolated nerve block (eg, digital, median, ulnar, or radial nerves), or brachial plexus block (eg, axillary, supraclavicular, or interscalene block). The choice of the technique will depend on the location and duration of the planned procedure, the need for tourniquet ischemia, and the skill and experience of the surgeon and the anesthetist. 30
Curr Probl Surg, January 2000
Intravenous Regional Anesthesia (Bier Block) Intravenous regional anesthesia is performed by filling the venous space of an extremity with local anesthetic solution after exsanguination of the limb and tourniquet ischemia. 92 The patient should have a pain-free condition of the hand, forearm, foot, or leg that requires surgery. The technique is limited to the upper extremity and the distal lower extremity. Only patients who can tolerate tourniquet ischemia are candidates for a Bier block. A 20- or 22-gauge catheter is placed in the most distal vein possible (usually hand vein). The upper extremity is exsanguinated first by gravity, and then the extremity is wrapped tightly, starting distally with an Esmarch bandage. A well-padded pretested double tourniquet is used. The distal tourniquet is inflated to a pressure 100 mm Hg above systolic pressure (200-250 mm Hg). Approximately 50 mL of 0.5% lidocaine without epinephrine is injected. The entire arm proximal to the distal tourniquet will be anesthetized. The distal tourniquet is elevated, and then the proximal tourniquet is deflated. The area under the proximal tourniquet is now anesthetized, permitting surgery for 2 hours without tourniquet pain. The tourniquet should not be deflated for at least 15 minutes after the local anesthetic is injected to minimize the risk of a toxic reaction to lidocaine. Although many anesthetists slowly release the tourniquet after the completion of the operation, there is no objective evidence that this technique reduces the risk of lidocaine toxicity. Regional anesthesia immediately ends on tourniquet deflation.
Digital Nerve Block The digital nerves are the terminal branches of the median and ulnar nerves that supply sensory innervation to the volar fingers and the dorsal fingers from the tips to the level of the proximal interphalangeal (PIP) joints. The digital nerves arise from the common digital nerves and are located on the volar radial and ulnar aspects of each finger, continuing distally. A dorsal sensory branch of each radial and ulnar digital nerve takes off dorsally just distal to the metacarpophalangeal joint and supplies the dorsal aspect of the finger from the tip to the PIP joint (Fig 8). Digital nerve blockade may be achieved at the base of each finger or in the intermetacarpal space. Approximately 0.5 to 1.0 mL of 1% Xylocaine without epinephrine is injected by inserting a 25- or 27-gauge needle at the volar base of each finger and angling the needle toward the radial and the ulnar side of the finger. Alternatively, the needle may be inserted through the interdigital skin dorsally and advanced volarly to the area of the nerve. Thin skin and less Curr Probl Surg, January 2000
31
2 ~il~Digital~rve
A
FIG 8. A, Technique of digital nerve block at the base of the finger. B, Techniquesof intermetacarpal nerve block. (From BridenbaughLD. The upper extremity: somatic block. In: CousinsMJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: JB Lippincott Company; 1988. p 387-416. By permission.)
sensitivity are the main advantages of the dorsal injection. The mandatory 2 needle sticks are a disadvantage. Care must be taken to avoid injection of excessive volumes of local anesthetic at the base of the finger to avoid a compartment syndrome and digital ischemia. Occasionally, a small volume of drug can be injected laterally over the dorsal sensory branches of the digital nerves to improve dorsal anesthesia, if required. Epinephrine should never be used with t h e local anesthesia for digital block because of the risk of digital ischemia. Some anesthetists prefer to inject the local anesthetic more proximally in 32
Curr Probl Surg, January 2000
~in Crease
Jlnaris Tendon
FIG 9. Median and ulnar nerve block. (From Bridenbaugh LD. The upper extremity: somatic block. In: Cousins M.,I, Bridenbaugh PO, editors. Neural blockade in clinical anesthesio and management of pain. 2nd ed. Philadelphia: JB Lippincott Company; 1988. p 387-416. By permission.)
the intermetacarpal space to achieve blockade of the common digital nerves because a higher volume of drug can be injected at this location with less risk of a compartment syndrome.
Median Nerve Block The median nerve supplies sensory innervation to volar digits 1 through 3 and the radial aspect of digit 4. Dorsally, the thumb is innervated from the interphalangeal joint distally and digits 2, 3, and radial digit 4 from the PIP joint distally. The median nerve can be blocked easily at the level of the wrist by injecting 5 mL of 2% Xylocaine into the carpal tunnel deep to the transverse carpal ligament (Fig 9). After sterile skin preparation, the patient is asked to oppose the thumb to the fourth finger and slightly flex the wrist. This maneuver will clearly identify the palmaris longus tendon, which lies superficial to the median nerve. The needle should be placed just ulnar to the palmaris longus tendon and angled 45 degrees distally. The anesthetist will usually "feel" the needle penetrate the transverse carpal ligament. A Curr Probl Surg, January 2000
33
Flexor
Ulnar Nerve I:1G 10. Ulnar nerve block. (From Bridenbaugh LD. The upper extremity: somatic block. In: Cousins MJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: JB Lippincott Company; 1988. p 387-416. By permission.)
small test injection should be made to ensure the needle is not in the nerve. No effort should be made to elicit paresthesia. The palmaris longus tendon is absent in approximately 20% of patients. In this case, the junction of the thenar and hypothenar eminence at the base of the palm marks the approximate position of the nerve, and the injection can be made just ulnar and proximal to this landmark in the wrist.
Ulnar Nerve Block The ulnar nerve innervates the ulnar portion of the palm, the ulnar side of the voiar fourth digit, and the volar fifth digit. The dorsal ulnar aspect of the hand and the fourth and fifth digits are also innervated by the dOrsal sensory branch of the ulnar nerve, which passes dorsally proximal to the wrist. The ulnar nerve may be blocked at the wrist or in the cubital tunnel. We prefer to block the ulnar nerve at the wrist because the cubital tunnel is a tight fascial compartment. There is a theoretic risk of a compartment syndrome if an excessive volume of drug is injected in this space. To block the ulnar nerve at the wrist, the patient is asked to extend the wrist and abduct the fingers. These maneuvers permit easy palpation of the flexor carpi ulnaris tendon. The ulnar nerve and ulnar artery lie deep to this tendon (Fig 10). The ulnar artery is located radial to the ulnar nerve. After sterile preparation of the skin, 5 mL of 2% Xylocaine is injected deep to the flexor carpi ulnaris tendon just proximal to the wrist. The needle should be inserted from the ulnar side to avoid injury to the artery. No effort should be made to try to elicit paresthesia. A small test injection is administered to ensure the needle is not within the nerve. A 15- to 20-minute walt is necessary to achieve adequate anesthesia (because of the size of the nerve). To block the ulnar nerve at the cubital tunnel, the patient is asked to 34
Curr Probl Surg, January 2000
extend the elbow and palpate the medial epicondyle. The cubital tunnel is located immediately posterior to the medial epicondyle. The ulnar nerve can often be palpated at this location. After sterile skin preparation, a 25or 27-gauge needle is inserted into the cubital tunnel, and 2 mL of 2% Xylocaine is injected. The drug should not be injected into the nerve. If a paresthesia is elicited, the needle should be repositioned before injection.
Peripheral Nerve Stimulation as an Aid to Peripheral Nerve and Nerve Plexus Block Motor responses to peripheral nerve stimulation may be helpful in locating both nerve plexuses and peripheral nerves and with motor neuron components during regional anesthetic procedures. 93 A peripheral nerve stimulator is not useful in pure sensory nerve blockade. The required equipment includes a constant current generator (nerve stimulator) and insulated needles. The needle is advanced with the stimulating current at approximately 1.0 mA. When a motor response is observed, the stimulating current is reduced incrementally, and the needle position is adjusted so that a motor response is elicited at a stimulating current of 0.5 mA or less. The lower the current required to elicit a motor response, the more likely the needle is in close proximity to the nerve. At this point, the local anesthetic solution is injected. The arguments in favor of using peripheral nerve stimulation during regional anesthetic as compared with the paresthesia technique include a reduction in patient discomfort and a possible reduction in the risk of n e r v e i n j u r y . 94 The disadvantages include the cost of the stimulator and the insulated needles.
Axillary
Block
The axillary block is used to provide anesthesia to the hand, forearm, and lower arm. It will not provide anesthesia for the shoulder and upper one third of the arm. The axillary block technique is based on the assumption that the terminal branches of the brachial plexus lie in a neurovascular bundle in close proximity to the brachial artery at the inferior aspect of the axilla. Three of the 4 terminal nerves of the brachial plexus usually are found within the fascial sheath. The radial nerve is located posterior to the brachial artery. The median nerve is found superior to the artery, and the ulnar nerve is located inferior to the brachial artery (Fig 11). The musculocutaneous nerve, the terminal branch of the lateral cord, takes off from the plexus near the coracoid process, passes through the coracobrachialis Curr Probl Surg, January 2000
35
Humerus~
Q Radialn.
J
Ulnarn.
FIG 11. Axillary block, a, Artery; n, nerve. (From Brown DL. Atlas of regional anesthesia. Philadelphia: WB Saunders Co; 1992. p 45. By permission.)
muscle, and therefore lies, for the most part, outside the neurovascular bundle. Injection of the local anesthetic into the fascial sheath may not block the musculocutaneous nerve, and a separate injection into the body of the coracobrachial muscle may be necessary to obtain complete anesthesia on the anterior aspect of the forearm. Patients with significant coagulation disorders are poor candidates for an axillary block because of the risk of hemorrhage into the fascial sheath and the development of a compartment syndrome. With the patient in the supine position and the ann extended on an arm board with the shoulder abducted and the elbow flexed, the anesthetist sits by the patient on the side to be anesthetized. There are several options for performing the block.
Transarterial Technique The brachial artery may be used as the endpoint for confirming entrance of the needle into the sheath. The needle is inserted through both walls of the artery and is withdrawn with continuous aspiration. After blood is obtained, the needle is readvanced through the posterior wall until blood 36
Curr Probl Surg, January 2000
is no longer aspirated. A small test dose of local anesthetic with epinephfine 1:200,000 to 1:400,000 is injected to confirm the extravascular position of the needle. A test injection is then made to ensure that intravascular injection does not occur. After the test injection, either the full dose of the drug is injected posterior to the artery or two thirds of the drug is injected posterior to the artery and the remaining one third of the drug is injected anterior to the artery. Alternatively, the perception of a palpable "click" can be used as evidence of the needle entering the fascial sheath of the neurovascular bundle. Unfortunately, there are many fascial layers in the arm and identification of the correct "click" takes a lot of experience and skill. Another approach is to use paresthesia as evidence of the presence of the needle within the fascial sheath. Although a paresthesia suggests the location of the needle to be within the sheath, a painful or burning sensation on injection may indicate an intraneural injection. The injection should be halted, and the needle should be withdrawn 1 to 2 mm. A reinjection should not elicit symptoms. A nerve stimulator may also be used to locate the brachial plexus and to guide needle placement. Another approach is to use a perivascular "field block" injection by injecting the drug in multiple sites around the brachial artery. Advocates of this approach argue that each nerve is contained in its own fascial compartment. 95 There are few objective data on which to base a recommendation of this technique. We prefer the use of the perivascular multiple injection and paresthesia techniques. The choices for local anesthetic include 1.5% to 2% Xylocaine and 1.5% to 2% mepivacaine. Epinephrine 1:200,000 or 1:400,000 can be added to prolong the block, decrease systemic absorption, and act as a marker of inadvertent vascular injection. Bupivacaine may be used for a longer acting block but may have a significantly longer onset of action compared to lidocaine and mepivacaine. A total of 20 to 40 mL of anesthetic solution is the typical dose for most adults, depending on the size of the patient.
Supraclavicular Block The supraclavicular block is indicated for surgery of the hand, forearm, and arm. This block usually provides inadequate anesthesia for shoulder surgery (Fig 12). The trunks of the brachial plexus lie between the anterior and middle scalene muscles just superior to the subclavian artery. The goal of the block is to inject the local anesthetic adjacent to the trunks of the brachial plexus, which are identified either by paresthesia or nerve stimulation. The 3 major potential complications of this block are pneumothorax, hematoma Curr Probl Surg, January 2000
37
CLAVICLE
FIG 12. Supradavicular block. (From grown DL. Atlas of regional anesthesia. Philadelphia: WB Saunders
Co; 1992. p 35. By permission.)
(because of subclavian artery puncture), and intravascular injection. The broad first rib functions as a "backstop" to prevent penetration of the pleura and injury to the cupola of the lung. Nevertheless, the risk of pneumothorax is 1% to 3% with this regional anesthetic technique. 96 The patient is positioned supine with the head turned towards the opposite shoulder. The anesthesiologist stands at the patient's head and inserts a 1.5-inch 22-gange needle attached to an extension tube and/or control syringe through a skin wheal made in the midclavicular line 1 cm posterior to the posterosuperior border of the clavicle. This point corresponds to the inferior base of the interscalene groove. The syringe is angled directly caudad and advanced slowly until either a paresthesia is elicited or the first rib is encountered. If a paresthesia occurs, the needle is aspirated for blood; and if none is obtained, a test dose of several milliliters of anesthetic is injected followed by incremental doses of the drug up to a total volume of 30 mL. If the rib is encountered without first obtaining a 38
Curr Probl Surg, January 2000
paresthesia, the needle is withdrawn just below the skin and reinserted in a sagittal plane taking care to follow the rib in small steps until the plexus is encountered. A nerve stimulator with the current set at 1 to 1.5 mA will help identify the plexus. If a muscle twitch occurs with the current reduced to 0.5 mA, the needle is most likely in close proximity to the plexus, and the local anesthetic solution may be injected. Two alternative techniques have been described. The "plumb-bob" technique was developed to reduce the risk of pneumothorax. 96 The needle is inserted at a 90-degree angle to the patient in the interscalene grove, midclavicular line, just lateral to the clavicular head of the sternomastoid muscle. Proponents of the plumb-bob technique argue that the needle is less likely to slide off the rib and injure the underlying lung with this approach. The third method of supraclavicular block is the subclavian perivascular approach. 97 A skin wheal is raised over the palpable subclavian artery above the clavicle. A 1.5-inch 22-gauge needle is inserted posterior to the palpable subclavian artery pulsation in a caudal direction. The anesthetic is injected when the correct needle position is confirmed by a nerve stimulator or a paresthesia. I (J.S.) prefer either the classic or the plumb-bob technique because the injection is made at right angles to the brachial plexus, making the identification of the plexus easier.
Interscalene Block The interscalene block is indicated for surgery of the upper extremity and shoulder. It may be used for hand surgery, although incomplete blockade of C8 and T1 (medial cord) usually requires supplemental ulnar nerve blockade. The block is performed far from the subclavian artery and the cupola of the lung, reducing the risk of subclavian injury and pneumothorax. However, the close proximity of the carotid and vertebral arteries and the epidural and subdural spaces may result in either hematoma formation or central neuraxial blockade. In addition, the presence of the stellate ganglion, the phrenic nerve, and the recurrent laryngeal nerve in the same anatomic area as the planned injection means that a temporary Homer's syndrome, hoarseness, and ipsilateral diaphragm paralysis are the usual consequences of an interscalene block. For this reason, an interscalene block should be used with caution in a patient with marginal pulmonary reserve. 98 The anesthesiologist stands at the patient's head or on the side to be blocked. The patient's head should be turned toward the contralateral shoulder. The patient is asked to elevate the head to identify the sterCurr larobl Surg, January 2000
3g
~rscelene iroove
,lefle m, plexus
FIG 13. Interscalene block. Ext, Exterior; Ant, anterior; m, muscle. (From Urmey WF. Upper extremity blocks. In: Brown DL, editor. Regional anesthesia and analgesia. Philadelphia: WB Saunders Co; 1996. p 254-78. By permission.)
nomastoid muscle lateral border. Posterior to the lateral border oLthe sternomastoid, the interscalene groove will be palpable, beginning at the level of C-6. A 1.5-inch 22-gauge needle is inserted perpendicular to the skin in the interscalene groove opposite the cricoid cartilage (C-6; Fig 13). The plexus is located within several millimeters of the skin at this level. The correct location of the needle is confirmed by paresthesia or muscle twitching with nerve stimulation. Deep injections (burying the needle to the hilt) should not be made because they increase the risk of central neuraxial blockade and/or intravascular injection. After aspiration, a test injection should be made, then an incremental injection of the anesthetic drug can be made. A total of 20 to 40 mL of drug is usually required, depending on the patient's lean body mass.
Stellate Ganglion Block Stellate ganglion block is commonly performed for the diagnosis and treatment of upper extremity complex regional pain syndromes (eg, causalgia, sympathetic dystrophies) unresponsive to more conservative treatment. Sympathectomy because of stellate ganglion block is also indicated in selected patients with diseases that cause upper extremity 40
Curr Probl Surg, January 2000
Common
Post. tubercle Ant. tubercle
Pmverlebr~ Longus colli m.
FIG 14. Stellate ganglion block, a, Artery; n, nerve; Post, posterior; Ant, anterior; m, muscle. (From Lamer TJ. Sympathetic nerve blocks. In: Brown DL, editor. Regional anesthesia and analgesia. Philadelphia: WB Saunders Co; 1996. p 357-84. By permission.)
ischemia such as Raynaud's disease, thromboangitis obliterans, frostbite, and levido reticularis. 99 There are 3 cervical sympathetic ganglia: the superior cervical ganglion adjacent to C1, the middle cervical ganglion adjacent to C6, and the inferior cervical ganglion, which is often fused with the first thoracic ganglion. This fusiform ganglion is called the stellate ganglion. It lies just anterior to the lateral process of C7 and T1 and is separated from the vertebra by the prevertebral muscles and fascia. Its anterior border is the carotid, subclavian, and vertebral arteries, and it is bounded inferiorly by the cupola of the lung. Blockade of the stellate ganglion results typically from caudad spread of local anesthetic from the point of injection, because the entry site of the needle is usually at the level of the middle cervical ganglion at C6. Injecting much lower than this may result in inadvertent arterial puncture or even pneumothorax, given the intimate association of the stellate ganglion with these structures. Typically, the well-sedated, but responsive patient is seated with the neck slightly extended and a small pillow or rolled towel supporting the neck. The cricoid cartilage is located by palpating inferiody along the trachea (Fig 14). The point of first widening is the cricoid cartilage. This is especially helpful Curr Probl Surg, January 2000
41
in women, in whom the larynx is not as prominent as in men. Lateral to this cartilage, one may palpate the anterior tubercle of the transverse process of C6 (Chassaignac's tubercle). The fingers of the noninjecting hand are placed between the trachea and the pulsation of the carotid artery, and the carotid is laterally retracted, while a 22-gauge needle is introduced directly posteriorly to contact with the C6 tubercle. The needle is withdrawn 1 to 2 mm, aspirated for blood, and if negative, a 1 to 2 mL test dose is injected. Inadvertent intravascular placement may result in immediate neurologic consequences because of the direct blood flow to the brain. If the test is negative, 5 to 10 mL of local anesthetic is injected. Because a dilute concentration of local anesthetic is all that is required to block sympathetic nerves and a longer rather than a shorter block is desirable, the agent typically used is 0.25% bupivacaine with epinephrine 1:200,000. Because of the close proximity of several major neural and vascular structures to the cervical ganglia, side effects are expected and, in fact, are confirmatory signs of a successful block. Although rare with careful technique, serious complications can occur. Side effects most commonly include Homer's syndrome and injection of the conjunctiva, nasal stuffiness, anhidrosis of the extremity, peripheral vasodilation, and increased skin temperature. Block of the recurrent laryngeal nerve is common, and the patient may experience hoarseness and even dyspnea. Occasionally, the somatic nerves of C5 to C7 are affected, resulting in motor and sensory block of the arm. Serious complications include hematoma, intravascular injection with seizures, and epidural or subarachnoid block. 1~176
Lower ExtremityNeural Blockade Local anesthetics are most commonly used for central neuraxial blockade to achieve anesthesia of the lower extremities. However, lower extremity neural plexus and peripheral nerve blocks may also be used. Unfortunately, anatomic considerations make these blocks more challenging than upper extremity blocks. Instead of a single tightly compact neural plexus coursing across easily palpable bony and vascular landmarks, the nerves supplying the lower extremity arise deep in the pelvis and either pass deep in the gluteal region or fan out immediately on entering the groin.
Lumbar PlexusAnatomy The nerves that form the lumbar plexus originate from the roots of LI to L4 (Fig 15). They exit the pelvis sandwiched between the psoas major and quadratus lumborum muscles. The lumbar plexus terminates in 3 nerves supplying the lower extremity: the obturator nerve, the femoral nerve, and the lateral femoral cutaneous nerve. 42
Curr Probl Surg, January 2000
\
:i
Qui~l~tus lumb0mm m.
femoral ~ltEmeous
n.
Femoral
P
f
\ /
// 8
spread
9
\
FIG 15. Lumbar plexus anatomy, m, Muscle; n, nerve. (From Brown DL. Atlas of regional anesthesia. Philadelphia: WB Saunders Co; 1992. p 75. By permission.)
The obturator nerve exits the pelvis through the obturator foramen and innervates the adductor muscles of the thigh and a palm-sized area of skin over the medial thigh. It terminates over the knee joint, supplying sensory innervation to a variable portion of the medial knee. For this reason, "femoral only" nerve blocks for knee arthroscopy may result in unsatisfactory anesthesia because of inadequate blockade of the portion of the knee innervated by the obturator nerve and the sciatic nerve from the lumbosacral plexus. Curr Probl Surg, January 2000
43
The femoral nerve arises at the lateral border of the psoas major muscle and exits the groin posterior to the inguinal ligament just lateral to the femoral artery. The nerve branches out like a fan in a highly variable fashion once it enters the groin. The femoral nerve provides motor innervation to the flexor muscles of the thigh and sensory innervation to the anterior thigh. The saphenous nerve, the terminal branch of the femoral nerve, supplies sensory innervation to the skin of the medial side of the knee, leg, and foot. The lateral femoral cutaneous nerve is exclusively a sensory nerve that innervates the lateral aspect of the thigh. The nerve passes subcutaneously 1 to 2 cm medial to the anterosuperior spine of the iliac crest. The options for blockade of the nerves supplied by L1 to IA include lumbar plexus blockade and separate blockade of the terminal branches of the lumbar plexus.
Lumbar Plexus Blockade The goal of lumbar plexus blockade is to fill either the paravertebral gutter at the level of L2 to L4 or the potential space between the psoas and quadratus lumborum muscles with local anesthetics to achieve anesthesia. Three techniques for lumbar plexus blockade are described. Lumbar Paravertebral Block. With the patient in the prone position, the needle is inserted at the upper lateral border of the L3 spinous process contacting the vertebra and then "walking off' the caudad side of the transverse process. The endpoint is either a paresthesia or contraction of the anterior or medial thigh muscles, if a nerve stimulator is used. A total of 30 mL of local anesthetic is injected after aspiration and injection of a small test dose. We rarely use this block in our practice because the patient must be in the prone position and there are more reliable alternatives. The "Three in One" Block. This block takes advantage of the fact that the lumbar plexus branches are sandwiched between the psoas and the quadratus lumborum muscles.I~ The needle is inserted at the level of the ilioinguinal ligament over the femoral nerve at the junction of the iliopsoas and iliacus muscles. The needle is advanced cephalad at a 45degree angle. Once the endpoint of a paresthesia or muscle twitch (with the nerve stimulator) is reached, the needle is aspirated, and a test dose is injected. A total of 30 mL of local anesthetic is injected forcefully to facilitate cephalad spread of the drug between the muscle planes. This technique is effective at blocking the femoral and lateral femoral cutaneous nerves but provides inconsistent blockade of the obturator nerve in our experience. The Psoas Compartment Block. This technique also makes use of the potential space between the psoas and quadratus lumborum muscles. With the patient in the prone position, the needle is inserted 5 cm lateral to the 44
Curr Probl Surg, January 2000
Sartoaus
Iliopsoas m.
l /,~,~,~. Peeline~l m.
. , / f
Femoral n/ ~
Femoral a.
I
Fascia
~,;":.":~.
FIG 16. Femoral nerve block, m, Muscle; lig, ligament; n, nerve; o, artery; v, vein. (From Rogers JN, RamomurthyS. Lowerextremityblocks. In: Brown DL, editor. Regional'anesthesiaand analgesia. Philadelphia: WB SoundersCo; 1996. p 279-91. By permission.)
spinous process of L2 or L3 perpendicular to the skin. The needle is advanced through the quadratus lumborum. When a loss of resistance is felt, the needle will be in the potential space between the quadratus lumborum and the psoas muscles. A nerve stimulator may be used to confirm the needle position. A total of 30 mL of local anesthetic solution is injected. '~ We rarely use this block because more convenient methods of lower extremity block are available.
Blockade of Peripheral Nerves Arising from the Lumbar Plexus Femoral Nerve Block. Twenty to 30 mE of local anesthetic is injected at the level of the inguinal ligament just lateral to the femoral artery (Fig 16). If a nerve stimulator is used, the local anesthetic is injected when quadricep contractions are obtained at 0.4 mA. Some anesthetists recomCurr Probl Surg, JanuarY 2000
45
mend making multiple injections lateral to the femoral artery because the nerve branches may begin to fan out at this level. Lateral Femoral Cutaneous Block. Blockade of the lateral femoral cutaneous nerve produces anesthesia on the lateral aspect of the thigh. Use of a nerve stimulator is not indicated because the lateral femoral cutaneous nerve is a pure sensory nerve. A total of 10 mL of local anesthetic is injected as a field block 2 to 3 cm medial to the anterior superior spine of the iliac crest. Obturator Nerve Block. The obturator nerve block is indicated for superficial surgery of the medial aspect of the thigh and knee. It is rarely performed as an individual nerve block. It is the deepest nerve of the lumbar plexus and the most difficult to approach and block effectively. Fortunately, it is not necessary to block this nerve for many surgical procedures. The knee is flexed, and the thigh is abducted. A long insulated needle is inserted 2 cm lateral and caudad to the pubic tuberal. The needle is advanced perpendicular to the skin until it hits the inferior border of the superior pubic ramus. The needle is "walked" off the superior pubic ramus, directing it in a posterolateral direction. With the nerve stimulator at a current of 2 to 3 mA, the needle is advanced until twitching of the adductor muscle occurs. The current is reduced to a level of 0.5 mA. If twitching continues, 20 mL of local anesthetic is injected. We rarely perform this block because it is uncomfortable for the patient and technically difficult. Lumbosacral Plexus Anatomy. The roots of L4 through $3 comprise the lumbosacral plexus, which gives rise to the sciatic nerve and its terminal branches, the common peroneal and tibial nerves. The sciatic nerve forms on the anterior aspect of the sacrum and exits at the sciatic notch, passing below the piriformis muscle and coursing in an arc across the buttock deep to the mass of gluteal muscles. The nerve then enters the thigh at a point halfway between the greater trochanter of the femur and the ischial tuberosity. The sciatic nerve courses in the midline posterior thigh caudad to a point just cephalad to the popliteal fossa where it divides into the common peroneal and tibial nerves. The tibial nerve continues posteriorly through the calf (supplying the plantar flexor muscles and skin), passes posterior to the medial malleolus, and splits into the medial and lateral plantar nerves (supplying the sole of the foot). The third terminal branch of the tibial nerve, the sural nerve, supplies sensory innervation to the lateral aspect of the foot. The peroneal nerve courses anterolaterally, crossing caudal to the head of the fibula where it is easily blocked with a few milliliters of local anesthetic. It supplies motor innervation to the foot dorsiflexor muscles and sensory innervation to the dorsum of the foot through its terminal branches, the superficial and deep peroneal nerves. 46
Curr Probl Surg, January 2000
Greater trochanter
3-5 cm ~
Piriformis m. ~atic
Posterior s u p .
n.
~ . " ~
FIG 17. Sciaticnerve block, m, Muscle;n, nerve;sup, superior.(From RogersJN, RamamurthyS. Lower extremityblocks. In: Brown DL, editor. Regionalanesthesiaand analgesia.Philadelphia:WB SaundersCo; 1996. p 279-91. By permission.)
Lumbosacral Plexus Block. The lumbosacral plexus may be blocked from the paravertebral approach. However, consistent neural blockade is difficult to achieve because of the large number of lumbar and sacral nerve roots that form the plexus.
Sciatic Nerve Block The sciatic nerve block is indicated for procedures that involve the lower extremity (usually in combination with a femoral nerve block). The classic approach was described by Labat. j~ With the patient in the Sims position, a triangle is drawn with the following vertices: the posterior superior iliac spine, the bony prominence of the greater trochanter, and the sacral hiatus just superior to the intergluteal fold. A line is drawn from the posterior superior iliac spine to the greater trochanter, and at the midpoint of that line a perpendicular line is drawn extending caudad 3 to 4 cm. If one then draws a line from the greater trochanter to the sacral hiatus, its midpoint should lie at the same point as the termination of the perpendicular line (Fig 17). A spinal needle or long insulated needle is then introduced Curr Probl Surg, January 2000
47
perpendicular to all planes of the skin and advanced until either a paresthesia or muscle twitch (plantar or dorsiflexion with nerve stimulation) is obtained. A total of 30 mL of local anesthetic is injected. The onset of action may be as long as 30 minutes because of the large size of the sciatic nerve. Many innovators of regional anesthesia have attempted to develop techniques of sciatic nerve block from either a lateral or anterior approach, thereby permitting both a femoral nerve and sciatic nerve block without a change in patient position. The anterior approach is based on the anatomic location of the nerve posterior to the neck of the femur, which lies posterior to the medial one third of the inguinal ligament. The anterior approach of Beck ~~ describes drawing a line from the greater trochanter parallel and inferior to the inguinal ligament. A second line is drawn from a point at the junction of the medial and middle thirds of the inguinal ligament caudad. The point o f intersection of the 2 lines is the site of insertion of a spinal needle perpendicular to all tissue planes. The needle is advanced with nerve stimulation until dorsal or plantar flexion muscle twitches are elicited. The lateral approach uses the greater trochanter as the primary landmark, 1~ but this block is difficult to perform and is rarely used.
Distal Lower Extremity Block The options for distal lower extremity blockade include the sciatic nerve block in the popliteal fossa through either the posterior or lateral approach, the saphenous nerve block, and the ankle block.
Popliteal Block of the Sciatic Nerve Posterior Approach. The patient is placed in the prone position with the leg fully extended. The needle is inserted perpendicular to the skin approximately 7 cm cephalad to the flexor crease in the popliteal fossa between the musculotendinous units Of the biceps femoris muscle laterally and the semitendinosis muscle medially (Fig 18). The needle is advanced with the stimulating current at 1.5 to 2.0 mA until plantar or dorsiflexion muscle twitches are elicited. The current is decreased to 0.5 mA to ensure proper needle position. A total of 30 to 40 mL of local anesthetic solution is injected) ~ LateralApproach. The patient lies supine with the leg extended. A 10cm-long 21-gauge insulated needle is inserted at a point 7 cm proximal to the lateral femoral epicondyle in the space between the vastus lateralis and the biceps femoris. The needle is advanced and angled posteriorly at a 30-degree angle. The needle is advanced with nerve stimulation until muscle twitches are elicited. Once muscle twitches in the distal extremity 48
Curr Probl Surg, January 2000
Sem~endinous m.
Sam
7."'
~ i u s
~a~al
n.
m.
FIG 18. Tib a nerve block, m, Muscle; n, nerve; Med, medial; Lat, lateral. (From RogersJN, RamamurthyS. Lowerextremity blocks. In: Brown DL, editor. Regional anesthesiaand analgesia. Philadelphia:WB Saunders Co; 1996. p 279-91. By permission.)
are elicited, the current is decreased to 0.5 mA, and the local anesthetic solution is injected. 1~
Saphenous Nerve Block The saphenous nerve may be blocked easily by injecting local anesthetic as a field block to the periosteum of the medial condyle of the tibia. Blocking this sensory nerve will provide anesthesia to the medial aspect of the lower leg and foot.
Ankle Block The most commonly performed lower extremity block is the ankle block (Fig 19). It is technically straightforward and provides reliable anesthesiato the foot. 1~ Five nerves must be anesthetized to achieve a complete ankle block: the posterior tibial nerve, the saphenous nerve, the superficial peroneal nerve, the deep peroneal nerve, and the sural nerve. The local anesthetic solution should not contain epinephrine. The block is begun by anesthetizing the posterior tibial nerve located at the posterior aspect of the medial malleolus. The nerve is in close proximCurt Probl Surg, January 2 0 0 0
4g
t~'~:l~
Saphenous v, and n, Tibialis ant.
Ext. hallucis Iongus tendon Deep peroneal n. and ant. tibial vessels \ ~ Ext, digitorum Iongus tendon
POSl. tibi~~
and n.
I
~i ~ 9~i84
~ngus
Me malle(
FIG 19. Ankle block, v, Vein; n, nerve; ant, anterior; Ext, exterior; Post, posterior; FI, flexor. (From Rogers JN, Ramamurthy S. Lower extremity blocks. In: Brown DL, editor. Regional anesthesia and analgesia. Philadelphia: WB Saunders Co; 1996. p 279-91. By permission.)
ity to the palpable posterior tibial artery. Five milliliters of local anesthetic solution is injected through a 25-gauge 1.5-inch needle with a fanning technique. The saphenous nerve is then anesthetized by injecting an additional 5 mL of local anesthetic solution subcutaneously just anterior to the medial malleolus. The deep peroneal nerve is anesthetized by injecting 5 mL of local anesthetic solution between the tendons of the tibialis anterior and extensor hallucis longus muscles at the level of the ankle. The superficial peroneal nerve passes superficial to the extensor retinaculum of the ankle. This nerve is blocked by injecting a subcutaneous ring of local anesthetic solution dorsally from the medial to the lateral malleolus. The sural 50
Curr Probl Surg, January 2000
nerve may be blocked by injecting 5 mL of local anesthesia subcutaneously midway between the lateral malleolus and the calcaneus.
Intercostal Block Intercostal blocks are useful for several indications. As a primary surgical anesthetic, this block can be combined with a celiac plexus block and be used for upper quadrant abdominal surgery. This is now rarely done because of the perceived ease and efficacy of general anesthesia and the increased use of laparoscopic techniques. The most corrffnon indications for intercostal block are for postoperative pain, analgesia for rib fractures, and herpes zoster pain. ~~ The primary rami of T1 through T11 constitute the intercostal nerves. Inferior to the ribs, the primary rami of T12 sends branches to the ilioinguinal and iliohypogastric nerves. Superiorly, a branch from T1 supplies the brachial plexus, and branches of T2 and T3 contribute to the intercostobrachial nerve, which innervates the skin of the medial aspect of the upper arm. Each intercostal nerve contains sympathetic and somatic fibers. The preganglionic white rami communicans supply fibers to the sympathetic chain, and the postganglionic sympathetic gray rami communicans travel to the intercostal nerve from the paravertebral sympathetic ganglion. The somatic component of the intercostal nerve branches at several points, which include the posterior cutaneous branch, the lateral cutaneous branch (arising anterior to the midaxillary line), and the anterior cutaneous branch (the termination of the nerve). The intercostal nerves lie within a sheath consisting of the pleura and the internal intercostal fascia. At the posterior angle of the rib, the nerve lies within a groove adjacent to the intercostal vein and artery. This close proximity of the nerve to the vascular structures and the pleura makes careful performance of the block a necessity because intravascular or intrapleural injections are distinctly possible. If one is blocking several intercostal nerves or is performing a bilateral intercostal nerve block for lower thoracic or upper abdominal surgery, a useful technique is to have the patient assume a prone position with the arms abducted to bring the scapulae as cephalad as possible; a pillow may be placed under the abdomen to reduce lumbar lordosis. The patient is sedated appropriately and receives nasal cannula oxygen. Pulse oximetry is advised. The spinous processes of the vertebrae corresponding to the ribs to be blocked are marked and connected with a line. The anesthesiologist moves laterally along the ribs to find the posterior angle of each rib and marks this point. Now, a line is drawn that connects the marks. This line should be parallel to the one connecting the spinous processes. The superior and inferior Curr Probl Surg, January 2000
51
FIG 20. Intercostal block. (From Thompson GE, Moore DC. Celiac plexus, intercostal and minor peripheral nerve blockade. In: Cousins MJ, Bridenbaugh PO, editors. Neural blockade in clinical anesthesiaand management of pain. 2nd ed. Philadelphia: JB Lippincott Company; 1988. p 503-30. By permission.)
margins of each rib are palpated and marked at the midpoint. The skin is prepared with povidone-iodine (Betadine) or other appropriate antiseptic; the local anesthetic is injected with a 25- or 27-gange needle subcutaneously at these points. Next, a 22,gange block needle attached to a control syringe is positioned at an angle perpendicular to the rib and advanced until the rib is contacted. The periosteum is infiltrated. The needle is withdrawn to just below the surface of the skin, and the syringe is angled slightly in a caudad direction. Recontact is made with the rib, and the needle is "walked" inferiofly until it slips off the inferior margin of the rib and falls 2 to 3 mm into the intercostal groove. This maneuver may be facilitated by first sliding the skin and subcutaneous tissue over the rib superiorly before placing the 22-gauge needle. As the rib is contacted, the tissue may be relaxed in the fingers and the elastic return of the skin will help "walk" the needle inferiorly. Once the needle is positioned correctly in the groove, the syringe is gently aspirated for blood, and 3 to 5 mL of local anesthetic solution (typically bupivacaine 0.5% with epinephrine 1:200,000) is injected. This process is repeated at each rib (Fig 20). 52
Curr Probl Surg, January 2000
For blocking a few ribs, such as in the case of a patient with rib fractures or with a chest tube, a midaxillary approach can be used, although the more anteriorly one blocks the rib, the greater the chance of missing more posterior branches. Several dye studies that have been performed in patients and latex cast studies that have been performed in cadavers have demonstrated the spread of local anesthetic in the costal groove and, despite the needle entry site, have revealed good spread throughout the nerve. ~~ Pneumothorax is the most feared complication with intercostal block, which causes many anesthesiologists to avoid performing this procedure. The actual incidence has been reported to be as low as a fraction of a percent.110 As for supraclavicular block, should pneumothorax occur, simple observation rather than an immediate chest tube is often adequate. Hematoma or, even more seriously, intercostal intrathoracic bleeding is possible with the block, and its performance should be avoided in patients with severe coagulopathies. A high blood level of local anesthetic is possible, given the large area of blood vessel exposed to local anesthetic. Careful attention to the volume and concentration of local anesthetic, the addition of epinephrine, and the number of ribs blocked are important to avoid systemic toxicity. 111 Because the blood level of the anesthetic continues to rise for the hour or so after the block are performed, observation of the patient is warranted when multiple rib blocks are performed. Finally, those patients who depend on their accessory muscles for breathing may not be good candidates for intercostal block because the motor block of the intercostal muscles may result in respiratory embarrassment. 112
Neuraxial Anesthesia The use of local anesthetics injected directly into the neuraxis (either epidural or subarachnoid space) is one of the most effective uses of these agents for surgery. Although the practice of neuraxial injection is now limited mostly to anesthesiologists, some surgeons (such as obstetricians) continue to perform these techniques.
Spinal Anesthesia Spinal anesthesia is practiced in much the same manner as Bier 113 first demonstrated the technique for surgery in 1899. A small amount of local anesthetic is injected into the subarachnoid space after entry into that space is confirmed by dural puncture with a styletted needle and subsequent visualization of free flow of CSF. Typically, the injection occurs at the lumbar interspaces below L2 because there is decreased risk of needle trauma to the substance of the spinal cord. The spinal cord usually ends at the inferior border of L1 in the adult and somewhat lower in the child at L2 to L3.1~4 Curr Probl Surg, January 2000
53
FIG 21. Spinal anesthesia. (From Stevens RA. Neuraxial blocks. In: Brown DL, editor. Regional anesthesia and analgesia. Philadelphia: WB Saunders Co; 1996. p 319-56. By permission.)
The patient is positioned in either the sitting position or more commonly the lateral decubitus position with the back rounded out to ensure as wide a vertebral interspace as possible. After identification of the appropriate interspace, typically either L4-5 or L3-4, and a sterile preparation and drape, the skin and subcutaneous tissues are infiltrated with local anesthetic. For a midline technique (most common), an introducer needle is advanced into the interspace, and then the styletted spinal needle is introduced through the introducer needle and advanced through the several layers of tissue and membranes until it is in the subarachnoid space. There is a characteristic feel of the penetration of both the ligamentum flavum and then the dura mater. The former membrane feels thicker and more elastic, whereas puncture of the dura mater yields a distinctive "pop" of the needle. At this point, the stylet is withdrawn, flow of CSF is observed, and the syringe containing the local anesthetic solution is attached to the hub of the needle. Gentle aspiration is performed to ensure the free flow of CSF, and the solution is then slowly injected into the subarachnoid space (Fig 21). LocalAnesthetic Solution. Local anesthetics in their usually manufactured concentrations and buffers are isobaric relative to CSE For spinal anesthesia, they can be manufactured or altered by the anesthetist to be either hyperbaric or hypobaric relative to CSE Hyperbaric solutions are made by the addition of 10% dextrose, and hypobaric solutions are made by the addition of sterile water. If an isobaric solution is desired, the anesthesiologist may simply use the commercially available solutions, provided they are preservative and additive free. Depending on the baricity of the local anesthetic injected, the patient is positioned in the appropriate manner for surgery. Hyperbaric solutions will sink. Therefore if the patient is in the sitting position and remains sitting after the injection of hyperbaric local anesthetic, the solution will 54
Curr Probl Surg, January 2000
TABLE 5. Duration of local anesthetic solutions in spinal anesthesia
Usual anesthetic duration prolongation by 0.2 mg eplnephdne
Agent Procaine Udocaine
Tetracaine
Bupivacaine
Usual concentration (%)
Usual volume (mL)
Badcity
Total dose (mg)
Minutes
10 1.5 5.0 2.0 0.5 0.1-0.3 0.5 0.5 0.75 0.5 0.75 0.25
1-2 34 1-2 2-4 1-4 2-10 1-4 2-4 1-3 2-4 1-3 34
Hyperbaric Hyperbaric Hyperbaric Isobaric Hyperbaric Hypobaric Isobaric Isobaric Isobaric Hyperbaric Hyperbaric Hypobadc
100-200 45-60 50-100 4080 5-20 6-20 5-20 10-20 7.5-22.5 10-20 7.5-22.5 7.5-10
3060 30-60 45-60 90-180 90-180 90-240 90-240 90-240 90-240 90-180 90-180 90-240
% 30-50 20-50 20-50 20-50 50-100 -50-100 20-30 20-30 20 20-30 --
Data from Concepcion M, Covino BG. Rational use of local anaesthetics. Drugs 1984;27:256-70; and from Lambert DH, Covino BG. Hyperbaric, hypebaric and spinal anesthesia. Resident and Staff Physician 1987;33:79-87. By permission. Table modified from Veering BT, Stienstra R. Duration of block: drug, dose and additives. Reg Anesth Pain Med 1998;23:352~5.
sink to anesthetize the lower sacral nerve roots. This will achieve the socalled "saddle block." If the patient remains in the lateral decubitus position, the "down side" will experience a denser block. This is often performed for hip surgery, before the patient is placed in the appropriate surgical position. If the patient is immediately placed supine, the local anesthetic will fall down either side of the sacral curvature and result in a higher block because one half of the anesthetic settles in the thoracic kyphosis, anesthetizing the lower and mid thoracic roots. The choice of local anesthetic depends on the desired duration of action of the anesthetic. The shortest-acting local anesthetic currently used is procaine, with a mean duration of approximately 45 minutes. The longest-acting local anesthetic is tetracaine, with a duration of up to 4 to 6 hours after a single dose, depending on whether epinephrine is added. More commonly, either lidocaine or bupivacaine is used. Lidocaine spinal blocks last, on average, for 1 to 1.5 hours, whereas bupivacaine spinal blocks last from 2 to 3 hours (Table 5). Duration of anesthetic times may vary depending on several factors, such as the addition of vasoconstrictors such as epinephrine, the baricity of the agent (ie, whether it is made hypobaric, isobaric, or hyperbaric relative to CSF), and the drug mass in milligrams injected. There has been some controversy recently focused on lidocaine Curr Probl Surg, January 2000
55
as a potential causative agent of "cauda equina syndrome," a neurologic deficit because of injury of the cauda equina. In the case of lidocaine, there have been several case reports that have implicated lidocaine as potentially neurotoxic, especially when used in higher concentrations (eg, commercially premixed at 5% with 7.5% dextrose) for hyperbaric spinal anesthesia. Although lidocaine is not the only anesthetic agent implicated in this syndrome, it has appeared in most of the cases reported. 115 Complications and Side Effects of Spinal Anesthesia. Spinal anesthesia leads to characteristic neurologic and physiologic changes, which variably last for the duration of the action of the local anesthetic. Some of these are clearly desirable such as complete sensory analgesia. Others may be desirable or of little consequence such as motor blockade, and others may be undesirable, such as hypotension and bradycardia caused by sympathetic nerve efferent blockade. Other possible side effects include urinary retention (particularly in men with prostatic hypertrophy), nausea, and dyspnea because of a blockade of intercostal muscles. 116 The most common complications of spinal anesthesia are backache and postdural puncture headache (spinal headache). 117Backache may be caused by direct muscle or bone trauma during the performance of the block or may be due to the relaxation of back muscles and subsequent ligamentous stretch while lying on a hard operating room table. Lithotomy position may exacerbate this. H8 Spinal headache results from the hole that may be left in the dura after dural puncture and the subsequent leak of CSE This creates 2 problems that may lead to a headache. First, there is loss of CSF and its cushioning effect on the brain and brainstem. There is a caudad displacement of these structures that stretches and aggravates the meninges. Second, loss of CSF leads to an increase in blood volume in the cerebral vessels, which leads to a "vascular" type headache, u9 Treatment for a spinal headache includes analgesics, hydration, and sometimes an "epidural blood patch" to cover and plug the hole. Some of the most significant advances in spinal anesthesia have been initiated to address the prevention of spinal headache and have occurred in needle design. It has been shown that increased needle diameter is directly proportional to increased risk of postdural puncture headache. 12~ This complication had, in the past, limited spinal anesthesia to those patients at the lowest risk of spinal headache, namely the elderly because there is a decreased incidence with increasing age. 117With the ability to manufacture smaller-diameter needles, the risk of spinal headache has decreased dramatically, from .as high as 20% to 30% to 1% to 4 % . 121 Another advance has been in needle-tip design. As opposed to "cutting" tip end-beveled needles, it was found that "pencil-point" needles with side orifices led to a 56
Curr Probl Surg, January 2000
decreased risk of spinal headache, presumably because these needles separated dural fibers rather than cut them, 122which in turn decreased the likelihood of a persistent leak of CSF. Other significant but extremely rare complications of spinal anesthesia include total spinal anesthesia, chemical or infectious meningitis, intrathecal or epidural bleeding with subsequent compressive hematoma and spinal ischemia, and direct nerve injury. A "total spinal" block occurs when the local anesthetic solution reaches the brainstem and may result in severe hypotension, apnea, and loss of consciousness. Treatment is supportive and involves managing the airway, oxygenation, and ventilation and maintaining the blood pressure with fluids and pressors until the effects of the spinal anesthetic wear off. Prevention of the other listed complications includes sterile technique, careful adherence to dosing guidelines, and avoidance of neuraxial block in the presence of bleeding or coagulation abnormalities and anticoagulants. Spinal Catheters. Aside from single injection spinal blocks, it is possible to introduce catheters into the subarachnoid space to achieve multiple dosing and therefore unlimited surgical time. Although the technique was pioneered in the 1940s by Lemmon, 123 its use has increased with the development of finer-gauge, high-tensile-strength catheters. However, as with lidocaine, the use of the ultrafine 27-gauge microcatheters has been implicated in cauda equina syndrome presumably because of maldistribution and resultant high concentrations of local anesthetic in the sacral c u r v a t u r e . 124 As a result, the 27-gauge microcatheter was withdrawn from the market by the United States Food and Drug Administration, although there are a variety of larger-diameter catheters still in common use.
Epidural Anesthesia Epidural anesthesia was independently codiscovered by Sicard and Cathelin 125of France in the early 1900s. Initially performed through the caudal epidural route, it is currently more commonly practiced in either the lumbar or thoracic region. The use of epidural anesthesia has greatly expanded in the past 20 years with the discovery of endogenous opioid receptors in the substance of the spinal cord. Although epidurally administered local anesthetics may provide complete surgical anesthesia, epidurally administered narcotics and dilute local anesthetic solutions have expanded epidural use beyond the operating room and into the postoperative recovery period for profound postsurgical analgesia. 126 Acute pain management services have greatly expanded in the past few decades largely because of the quality of analgesia provided by the epidural route. Epidural Technique. Local anesthetics can be administered at any level Curr Probl Surg, January 2000
57
of the epidural space, from the foramen magnum superiorly to the caudal canal inferiorly. Similar to the positioning used for spinal blocks, a patient may be in the sitting or in the lateral decubitus position for the procedure. After sterile preparation and drape, the skin and deeper subcutaneous tissue over the proposed interspace is infiltrated, and a styletted epidural needle (such as an 18-gauge Tuohy or Crawford) is introduced in either the midline or the paramedian orientation. It is more common to enter from the midline in the caudal, lumbar, and cervical interspaces because of the orientation of the spinous processes, which are nearly perpendicular to the axis of the back. The thoracic spinous processes are angled more acutely; therefore a paramedian approach to the space is often warranted. The needle is advanced until the ligamentum flavum is contacted. This is performed by tactile sensation. The "loss of resistance" technique involves attaching a 3-, 5-, or 10-mL glass syringe with a few milliliters of sterile saline solution and a small amount of air to the hub of the epidural needle after withdrawing the stylet. The nondominant hand then slowly guides the needle through the ligamentum flavum, while the thumb of the dominant hand exerts continuous pressure on the plunger of the syringe. There will be an immediate loss of resistance on the plunger once the needle has exited the far side of the ligamentum flavum and has entered the epidural space (Fig 22). It is important to maintain fine-needle control because only a few millimeters and a thin dura mater separate this space from the subarachnoid space. Puncture of the dura mater with the epidural needle results in a "wet tap" and a large hole in the dura, which almost invariably leads to a spinal headache. Epidural Test Dose. Once the needle is in the correct position, either a 20-gauge epidural catheter is threaded several centimeters into the epidural space or the local anesthetic injection can be made directly through the needle. Regardless of which option is selected, a test dose must first be administered. Typically this consists of 3 mL of local anesthetic combined with 15 p.g of epinephrine. The purpose of the test dose is to ensure that the local anesthetic is injected into the epidural space rather than the subarachnoid space or intravascularly. The components of the test dose are designed to detect the latter occurrences. 127 Should the test dose enter the subarachnoid space, the patient will experience a rapid onset of anesthesia consistent with an isobaric spinal block. Should the test dose enter a blood vessel, the 15 p.g of epinephrine is enough to raise the heart rate 15 to 45 beats above the baseline within 30 seconds. If a test dose is positive, the epidural needle or catheter should be removed, and the decision of whether or not to proceed with the epidural anesthetic must be made. Typically, a subarachnoid injection of 58
Curr Probl Surg, January 2000
/
'Y//
S FIG 22. "Bromage grip" for epidural block. (From Stevens RA. Neuraxial blocks. In: Brown DL, editor. Regional anesthesiaand analgesia. Philadelphia: WB SoundersCo; 1996. p 319-56. By permission.)
the test dose calls for abandoning an epidural technique, whereas an intravascular injection calls for repeating the procedure at another interspace. Again, a new test dose is carried out because failure to perform a test dose can lead to a massive subarachnoid or intravascular dose of local anesthetic. Curr Probl Surg, January 2000
59
Local Anesthetic Solution. As opposed to spinal anesthesia, where smaller amounts of local anesthetic are used to provide anesthesia, higher drug masses are used in epidural anesthesia because the dura mater acts as a barrier to diffusion of local anesthetic. Additionally baricity of local anesthetic solution is not a consideration because the epidural space is a potential space and does not contain a liquid medium. One must ensure that the local anesthetic administered is formulated for the epidural space and does not contain preservatives or additives. A short, intermediate, or long-acting local anesthetic may be used. Examples include 2% to 3% 3-chloro-procaine, 1.5% to 2% lidocaine, 0.25% to 0.75% bupivacaine, or 0.2% to 1.0% ropivacaine. Depending on the level of the injection (ie, caudal, lumbar, thoracic, or cervical) anywhere from 3 to 25 mL of local anesthetic is injected. Total drug mass (ie, volume • concentration) is the most important determinant of the quality of the block and its dermatomal extent. 128 Higher-concentration local anesthetics in higher volumes will lead to more profound surgical blocks of greater area and more complete motor blockade, whereas dilute concentrations of local anesthetics of lower volume may result in analgesia with greater motor nerve function. Typically the higher-concentration blocks are used for surgery, whereas dilute infusions of local anesthetics combined with opiates are used for postoperative pain management. Complications and Side Effects of Epidural Anesthesia. Because of the larger drug mass required for epidural anesthesia, systemic complications of local anesthetics are a significant issue. The use of test dosing as noted earlier and an awareness of the total dose of drug administered are important to ensure that toxic blood levels of local anesthetic do not occur. Like spinal anesthesia, high block levels will result in sympathectomy and a subsequent decrease in the blood pressure and potentially the heart rate. Unlike spinal anesthesia, however, the spread of local anesthetic is limited to the upper cervical spine because of the anatomic boundaries of the epidural space. Thus a "total spinal" block is an extremely rare occurrence, unless significant amounts of local anesthetic diffuse or leak into the subarachnoid space. Similarly, postdural puncture headache does not occur unless the dura is pierced or torn inadvertently. Backache may result from mechanical trauma. Additionally, older formulations of 3-chloroprocaine were implicated in causing back pain presumably as the result of the preservative methylparaben. Newer formulations are methylparaben free.129 Other complications of epidural anesthesia are similar to those for spinal anesthesia and include neural injury, infection, and bleeding. The latter complication is of special concern with epidural anesthesia because 60
Curr Probl Surg, January 2000
of the extensive vascular plexus of the epidural space and the confined space. Uncontrolled bleeding within the epidural space can lead to compressive ischemia of the spinal cord and nerve roots, resulting in complications that include loss of bowel and bladder function, paraplegia, quadraplegia, and even death. ~3~The recent introduction of the low molecular-weight heparins has resulted in an unusually high number of cases of epidural hematoma after neuraxial anesthesia. Because of the greater recognition of the need of perioperative thromboprophylaxis and the increased use of newer agents that are more potent anticoagulants, extreme vigilance is required on the part of anesthesiologists and surgeons about which patients are not suitable for neuraxial anesthesia. The US Food and Drug Administration has recently required "Black Box" warnings on all of the low-molecular-weight heparins, and several advisory committees have been created to address these concerns and to issue guidelines. ~31
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82.
83. 84. 85. 86. 87.
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