MANUAL OF REGIONAL ANESTHESIA

Transcription

1 MANUAL OF REGIONAL ANESTHESIA Carlo D. Franco, MD Chairman Orthopedic Anesthesia JHS Hospital of Cook County Associate Professor Anesthesiology and Anatomy Rush University Medical Center Chicago, IL Second Edition 2007

2 This manual is intended for the Anesthesiology Residents and Faculty of the Department of Anesthesiology and Pain Management of Cook County Hospital. With the exception of chapters on peripheral nerve blocks, which are written from the author s direct experience, the rest of the material comes from his understanding and interpretation, including actual quote, of the available literature. The author made every effort to give proper credit to the sources. The persons depicted in the pictures, models and patients, gave their written permission to the author to have their photographs taken and used for the purpose of teaching. Their decision was voluntary and did not involve compensation of any kind. The photographs of cadaver material depicted in this manual come from dissections performed by the author in the Anatomy Laboratory, Rush University Medical Center in compliance with Rush University, State and Federal laws and regulations. Care was taken to confirm the accuracy of the information presented in this manual. However the author is not responsible for errors or omissions or for any consequences from application of the information and techniques in this manual and makes no warranty, expressed or implied, with respect to the contents of it. This manual is in accordance with current recommendations as of April However recommendations and guidelines change so the reader is urged to check for new indications, warnings and precautions. This manual was produced with the author s personal funds. No departmental or grant money was used. 2

3 To my residents, who make my coming to work intellectually challenging and pleasurable and to the memory of my father 3

4 Chapter 1 Chapter 2 Chapter 3 Chapter 4 Chapter 5 Chapter 6 Chapter 7 Introduction Local Anesthetics Neuraxial Anesthesia Regional Anesthesia and Anticoagulation Peripheral Nerve Blocks Upper Extremity Blocks Lower Extremity Blocks 4

5 CHAPTER 1 INTRODUCTION General considerations.. 6 Patient selection and premedication...6 Monitoring...7 Outcome issues... 7 References 10 5

6 General considerations Regional anesthesia (neuraxial and peripheral nerve blocks) involves the anesthesia of an area of the body (e.g., upper extremity) without necessarily affecting the patient s level of consciousness. The practice of regional anesthesia is increasingly popular in the United States and around the world. The recent introduction of ultrasound to assist peripheral nerve blocks has started a new and exciting chapter in our subspecialty where new technology is helping to make our practice more objective and rational. In this manual I discuss several aspects related to the performance of regional anesthesia according to the techniques most commonly used in the United States, but with special emphasis in the techniques we perform daily at Cook County Hospital. Regional anesthesia has been traditionally considered an art. As such, it is usually practiced by artists who use their particular talents to produce results difficult to reproduce by non-artistic anesthesiologists. We have enormous respect for all the pioneer practitioners who introduced and/or popularized the various regional anesthesia techniques available to us now. We owe them a debt of gratitude. However in the 21 st century we should take advantage of all the technology available to us and favor science over art when practicing regional anesthesia. The blocks that we perform and which I describe in these pages are based mainly on facts (e.g., anatomical, physiological, and pharmacological). The endpoints chosen are objective and the local anesthetic solutions are used in volumes and concentrations considered adequate by clinical experience. After controlling all possible factors we expect our results to be predictable and reproducible. Regional anesthesia carries the risks and complications associated with use of local anesthetics (i.e., local anesthetic toxicity), the risks and complications of using needles and drugs in the proximity of nerves (e.g., neuropraxia, irreversible nerve damage) and those risks associated with a particular technique (e.g., pneumothorax, total spinal, etc). As with any other anesthetic technique, choosing regional anesthesia requires a thorough assessment that should include the patient, the surgeon, the nature of the procedure and its estimated duration as well as the level of experience of the anesthesiologist with regional anesthesia and its management. Patient selection and premedication The type of anesthesia for any procedure must be tailored to every individual patient. There are patients who in general are not good candidates for regional anesthesia especially if they remain awake (e.g., drug abusers, pediatric patients). On the other hand we have a vast and successful experience with peripheral nerve blocks on drug abusers and some pediatric patients, confirming that each case must be individually evaluated. Judicious use of sedation increases patient s cooperation and acceptance. Sedation should be used to calm anxiety, but not to turn the patient unconscious or otherwise unresponsive. This is especially true in blocks performed close to the neuraxis like interscalene blocks and lumbar plexus blocks. Keeping the patient lightly sedated, but awake and cooperative makes the procedure easier for both the patient and the anesthesiologist. A conscious and cooperative patient may also decrease the chances for 6

7 complications (e.g., pain at injection, early subjective symptoms indicating impending systemic toxicity, etc). Monitoring Every nerve block, whether it is performed in holding area, OR, PACU or office must be treated as potentially dangerous. Monitoring blood pressure, heart rate and pulse oxymetry as well as the establishment of IV access must always be considered. Supplemental oxygen should be given especially when sedation is being used. Resuscitation equipment, including oxygen, ambu bag, airways of different sizes, intubation equipment and tubes along with appropriate resuscitation drugs must always be readily available. A clear strategy to deal and treat complications must be in place. It is always advisable before starting a technique to leave room at the head of the bed for the anesthesiologist to manage the patient s airway in case this becomes necessary. Familiarity with the surroundings helps when dealing with emergencies. Outcome Is regional anesthesia safer than general anesthesia? Every discussion on regional anesthesia must address the issue of its relative safety compared to general anesthesia. Despite several studies suggesting it and an intuitive feeling that regional anesthesia seems safer than general anesthesia, no definite and general answer can be given. First of all most of the outcome studies have compared the relative benefits of neuraxial anesthesia (spinal or epidural) versus general anesthesia in intra abdominal surgery. Most of the studies lack the power (number of cases) to be able to see a true difference, if there is one, and most of them are retrospective. Lack of randomization raises the possibility of bias at the time of technique selection (e.g., sicker patients might have received regional anesthesia more frequently, thus making the comparison with general anesthesia more complicated). Other problems have to do with the parameter chosen for comparison. If mortality is chosen the populations to study would have to be extremely large to find a statistically significant difference since mortality under anesthesia is extremely low. Other parameters like DVT, myocardial infarction, pneumonia seem more adequate for comparison but their rates vary according to the procedure and not just type of anesthesia. If physiological parameters are measured (e.g., PO2, O2 sat) there is evidence that these numbers are frequently better after regional than general anesthesia, however their impact on morbidity is not clear. Nonetheless, there is some degree of agreement that in certain procedures regional anesthesia improves the outcome in a number of different ways like decreased rates of DVT, PE and blood loss. Surgeries most associated with improved outcome after regional anesthesia include: 1. Hip Surgery (hip fracture surgery and total hip arthroplasty): rates of DVT, PE and blood loss are reduced after neuraxial anesthesia. The mechanism is unknown, but may involve better peripheral circulation and less stasis. 7

8 Mortality rates have been shown to be significantly lower with epidural anesthesia as compared to general anesthesia. 2. Total knee arthroplasty: rates of DVT and PE are lower with neuraxial anesthesia. 3. Prostatectomy: similar reduction, possibly by a similar mechanism. 4. Peripheral vascular surgery: epidural anesthesia and postoperative epidural analgesia have shown to improve graft patency after peripheral vascular surgery, but does not seem to improve outcome after intra-abdominal vascular surgery. Mechanism is not clear. Improve runoff due to vasodilatation or preservation of normal coagulation has been mentioned. 5. Colon surgery: postoperative thoracic epidural analgesia with local anesthetics has shown to enhance colonic activity after colon resection. If narcotics are used in conjunction with local anesthetics this beneficial effect is lost. Procedures were regional anesthesia has not shown benefits as compared to general anesthesia include: 1. Upper abdominal and thoracic surgery, this is despite the fact that better pain scores and times to extubation can be obtained. 2. Upper and lower extremity surgery: even though the patients may have a higher degree of satisfaction and fewer side effects (nausea and vomiting) especially immediately after surgery. This difference rapidly disappears at 24 h. Airway and regional anesthesia For some anesthesiologists managing a difficult airway usually means securing it. This approach negates the benefits that regional anesthesia can provide when it is used along with judicious amount of sedation. In our practice we have provided upper extremity blocks to patients wearing halos and cervical collars when in our judgment the advantages have outweighed the risks. For more details please read Nigel Sharrock s chapter 2, Risks-Benefit Comparison for Regional and General Anesthesia, In: Complications of Regional Anesthesia, edited by Brendan T. Finucane. An interesting study was published in December 2000 in the British Medical Journal (not an anesthesiology journal) by Rodgers et al from New Zealand. The authors reviewed the literature looking for randomized trials with or without use of neuraxial anesthesia (spinal or epidural) before A total of 141 trials including 9,559 patients were included in this meta-analysis. The following are the main findings: 1. Overall mortality was about one third less in the neuraxial group (103 deaths/4871 patients versus 144/4688 patients, P=0.006). This decrease was observed regardless whether neuraxial was used alone or in combination with general anesthesia. 2. DVT decreased by 44% 3. PE decreased by 55% 4. Transfusion requirement decreased by 50% 5. Pneumonia decreased by 39% 8

9 6. There were also reductions in myocardial infarction and renal failure. The authors concluded, Neuraxial blockade reduces postoperative mortality and other serious complications, adding that it is not clear whether these effects are due solely to benefits of neuraxial blockade or partly to avoidance of general anaesthesia. Meta-analysis has the advantage of pooling large numbers so clinical events that are infrequent can be studied. However it means putting together trials from different institutions, including in some cases from different countries and different cultures. It remains to be seen whether these very encouraging results can be duplicated and whether they would apply more generally to regional anesthesia beyond neuraxial blocks (i.e., peripheral nerve blocks). Christopher Wu, from Johns Hopkins has shown the benefits of regional anesthesia over general when non-traditional outcomes (other than morbidity and mortality) like patient satisfaction, pain scores and the alike are measured. These socalled soft parameters are having increased importance in today s practice. 9

10 References 1. Sharrock NE: Risk-benefit comparisons for regional and general anesthesia in: Complications of regional anesthesia. Edited by Finucane BT. New York, Churchill Livingstone, 1999, pp Wu C. ASA Newsletter, May Rodgers A, Walker N, Schung S et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomized trials. Br Med J, 2000; 321:

11 CHAPTER 2 LOCAL ANESTHETICS Definition and historical perspective...12 Chemical structure..13 Structure-activity relationship..13 Mechanism of action and Na + channels...14 Frequency and voltage dependence. 15 Pregnancy and local anesthetics..15 Fiber size and pattern of blockade...15 Modulating local anesthetic action..16 Local anesthetics additives.. 17 Extended-release morphine.19 Clonidine.19 Dexmedetomidine...20 Neostigmine and NMDA antagonists..20 Metabolism...20 Dibucaine number 21 Toxicity Tumescent anesthesia...22 Toxic plasma concentrations 23 Toxicity management...23 Lipid emulsion.23 Maximum dose.25 Methemoglobinemia 25 Allergy 25 Characteristics of some individual agents 26 References 29 11

12 LOCAL ANESTHETICS The cell membrane s resting potential is negative and close to the potential determined by potassium alone (-70 mv). During the transmission of an action potential, Na + moves into the cell through open Na + channels depolarizing the membrane (potential raises to -20 mv or more). Local anesthetics are compounds with the ability to interrupt the transmission of the action potential in excitable membranes. They bind to specific receptors in the Na + channels and their action at clinically recommended doses is reversible. Conduction can still continue, although at a slower pace, with up to 90% of receptors blocked. All local anesthetics are neurotoxic if injected intraneurally and the damage caused is directly related to the degree of hydrostatic pressure reached inside the axoplasma. Local anesthetics injected around nerves could also be toxic as result of the concentration of the agent and the duration of the exposure (e.g., cauda equina after intrathecal local anesthetics). The local anesthetics available in clinical practice are usually racemic mixtures (a mix of both R and S enantiomers); exceptions are lidocaine, levo-bupivacaine and ropivacaine. The S isomer appears to have similar efficacy than the R isomer but lesser cardiac toxicity. Historical perspective Anesthesia by compression was common in the antiquity. Cold as an anesthetic was widely used until the 1800s. The native Indians of Peru chewed coca leaves and knew about their cerebralstimulating effects. The leaves of erythroxylon coca were taken to Europe where Niemann isolated cocaine in Germany in In 1884 in Austria Carl Koller, a contemporary and friend of Sigmund Freud is credited with the introduction of cocaine as a topical ophthalmic local anesthetic. In 1888 Koller came to the US and established a successful ophthalmology practice at Mount Sinai Hospital in New York until the year of his death in Recognition of cocaine s cardiovascular side effects as well as its potential for dependency and abuse led to a search for better local anesthetic drugs. Other highlights related to local anesthesia are: 1850s Invention of the syringe and hypodermic hollow needle Halsted, an American surgeon, blocks the brachial plexus with a solution of cocaine under direct vision (surgical exposure) Wood in the United Kingdom is credited with the introduction of conduction anesthesia through hypodermic injection Epinephrine is isolated by John Abel at Johns Hopkins Medical School Braun in Germany relates cocaine toxicity with systemic absorption and advocates the use of epinephrine Bier is set to receive the first planned spinal anesthesia from his assistant Hildebrandt, who gets CSF but cannot inject because the syringe doesn t fit the needle. Dr Bier then performs the first spinal anesthesia on Dr Hildebrandt using cocaine. They both experience the first spinal headaches Bier introduces the IV block (Bier block) with procaine. 12

13 1911 Hirschel performs the first percutaneous axillary block Kulenkampff performs the first percutaneous supraclavicular block Gaston Labat, Frenchman and disciple of Pauchet, introduces in the United States his book Regional Anesthesia Its Technic and Clinical Application. Labat founded the first American Society of Regional Anesthesia Daniel Moore from Virginia Mason Clinic in Seattle publishes his book Regional Block. It soon became the standard book in Regional Anesthesia Alon Winnie along with L. Donald Bridenbaugh, Harold Carron, Jordan Katz, and P. Prithvi Raj establish the current American Society of Regional Anesthesia (ASRA) in Chicago The first ASRA meeting is held in Phoenix, Arizona Regional Anesthesia Journal, volume 1, number 1 is published Alon Winnie s book Plexus Anesthesia, Perivascular Techniques of Brachial Plexus Block is published. Date of introduction in clinical practice of some local anesthetics: 1905 procaine; 1932 tetracaine; 1947 lidocaine; 1955 chloroprocaine (last ester type local anesthetic introduced that is still in clinical use); 1957 mepivacaine; 1963 bupivacaine; 1997 ropivacaine; 1999 levobupivacaine. Chemical structure of local anesthetics Local anesthetics are weak bases with a pka above 7.4 and poorly soluble in water. They are commercially available as acidic solutions (ph 4-7) of hydrochloride salts, which are hydrosoluble. A typical local anesthetic is composed of two moieties, one a benzene ring (lipid soluble, hydrophobic) and the other an ionizable amine group (water soluble, hydrophilic), linked by a chemical chain. This chemical chain can be either of the ester (-CO-) or amide types (-HNC-) defining two different groups of local anesthetics, esters and amides. Injecting local anesthetics in the proximity of a nerve(s) triggers a sequential set of events that eventually leads to interaction of some of their molecules with receptors located in the Na + channels of nerve membranes. The injected local anesthetic volume spreads initially by mass movement, moving across points of least resistance, which do not necessarily lead into the desired nerve(s), stressing the importance of injecting in proximity of the target nerve(s). The local anesthetic solution then diffuses through tissues; each layer acting as a physical barrier and in the process part of the solution gets absorbed into the circulation. Finally a small percentage of the anesthetic reaches the target nerve membrane at which point the different physicochemical properties of the individual anesthetic will dictate the speed, duration and nature of the interaction with the receptors. Physicochemical properties-activity relationship 1. Lipid solubility: determines both the potency and the duration of action of local anesthetics by facilitating their transfer through membranes and binding the drug close to the site of action and thereby decreasing the rate of metabolism by plasma esterase and liver enzymes. In addition, the local anesthetic receptor site in Na + channels is thought to be hydrophobic, so its affinity for hydrophobic drugs is 13

14 greater. Hydrophobicity also increases toxicity, so the therapeutic index of more lipid soluble drugs is decreased. 2. Protein binding: local anesthetics are bound in large part to plasma and tissue proteins. The bound portion is not pharmacologically active. The plasmatic unbound fraction is responsible for systemic toxicity. The most important binding proteins in plasma are albumins and alpha-1-acid glycoprotein (AAG). Although albumin has a greater binding capacity than AAG, the latter has a greater affinity for drugs with pka higher than 8 like most local anesthetics. Newborn infants have very low concentration of AAG reaching adult values by 10 months of age. The elderly and debilitated usually have some decreased levels of albumin and other plasma proteins (increased potential for toxicity). AAG levels increase during stress and for several days after the postoperative period. Their higher levels will decrease the unbound portion of local anesthetics leading to a potential decrease in local anesthetic toxicity. However changes in protein binding are only clinically important for drugs highly protein bound such as bupivacaine, which is 96%, bound (Br J Anaesth 1996; 76:365-8). The fraction of drug bound to protein in plasma correlates with the duration of action of local anesthetics: bupivacaine = ropivacaine > tetracaine > mepivacaine > lidocaine > procaine (5%) and 2-chloroprocaine (negligible). This suggests that the bond between the local anesthetic molecule and the sodium channel receptor protein may be similar to that of local anesthetics binding to plasma protein (similar amino acid sequences). Drugs as lidocaine, tetracaine, bupivacaine and morphine (e.g., DepoDur) have been incorporated into liposomes to prolong their duration of action. Liposomes are vesicles with two layers of phospholipids, which slow down the release of the drug. 3. Pka: determines the ratio between the ionized (cationic) and the uncharged (base) forms of the drug. The pka of local anesthetics ranges from 7.6 to 9.2. By definition the pka is the ph at which 50% of the drug is ionized and 50% is present as a base. The pka generally correlates with the speed of onset of most local anesthetics. The closer the pka is to the physiologic ph the faster the onset (e.g., lidocaine with a pka of 7.7 is 25% non-ionized at ph 7.4 and has a more rapid onset of action than bupivacaine with a pka of 8.1 which is only 15% nonionized). One important exception is 2-chloroprocaine with a pka of 9.0 and very short onset. This fast onset could be related to its low toxicity, which allows for high concentrations to be used clinically. It is also claimed that 2-chloroprocaine has better tissue penetrability. Mechanism of action and sodium channels The non-charged hydrophobic fraction (B), which exists in equilibrium with the hydrophilic charged portion (BH + ), crosses the lipidic nerve membrane and initiates the events that lead to Na + channel blockade. Once inside the cell, the pka of the drug and the intracellular ph dictate a new equilibrium between the two fractions. Because of the relative more acidic intracellular environment, the relative proportion of charged fraction (BH + ) increases. This fraction is the ultimate active form in the Na + channel. 14

15 The Na + channel is a protein structure that communicates the extracellular of the nerve with its axoplasm and consists of four repeating alpha subunits, plus beta-1 and beta-2 subunits. The alpha subunits are involved in ion movement and local anesthetic activity. It is generally accepted that the main action of local anesthetics involves interaction with specific binding sites within the Na + channel. Local anesthetics may also block to some degree calcium and potassium channels as well as N-methyl-Daspartate (NMDA) receptors. Local anesthetics do not ordinarily affect the membrane resting potential. The Na + channels seem to exist in three different states, closed (resting), open and inactivated. With depolarization the protein molecules of the channel undergo conformational changes from the resting state to the ion-permeable state or open state allowing the inflow of extracellular Na +, which depolarizes the membrane. After a few milliseconds the channel goes then through a transitional inactivated state where the proteins leave the channel closed and ion-impermeable. With repolarization the proteins revert to their resting configuration. Other drugs like tricyclic antidepressants (amitriptyline), meperidine, volatile anesthetics and ketamine also exhibit Na + channel-blocking properties. Tetrodotoxin and other biotoxins also interact with the Na + channels although their action is exerted on the extracellular side of the channel. Frequency and voltage dependence Local anesthetics show more affinity for open channels (frequency-dependent blockade) whereupon their effect on Na + channels increases with increased frequency of depolarization (e.g., pain or voluntary muscle contractions). In other words, a firing nerve is more sensitive to blockade. The degree of block also depends on the nerve resting membrane potential, a more positive membrane potential causes a greater degree of block (voltage-dependent blockade). Pregnancy and local anesthetics Increased sensitivity to local anesthetics (more rapid onset and more profound block) may be present during pregnancy. Also alterations in protein binding of bupivacaine may result in increased concentrations of active unbound drug in the pregnant patient. Placental transfer is more active also for lipid soluble local anesthetics, whereas higher protein binding becomes an obstacle to such transfer. In any case, agents with a pka closer to physiologic ph have a higher placental transfer. For example the umbilical vein/maternal vein ratio for mepivacaine is 0.8 (pka 7.6) while for bupivacaine is 0.3 (pka 8.1). In the presence of fetal acidosis, local anesthetics cross the placenta and become ionized in higher proportion than at normal ph. As ionized substances they cannot cross back to the maternal circulation ( ion trapping ). Thus, 2-chloroprocaine with its very short maternal and fetal half-lives is theoretically an ideal local anesthetic in the presence of fetal acidosis. Fiber size and pattern of blockade As a general rule small nerve fibers are more susceptible to local anesthetics than large fibers. However other factors like myelinization and relative position of the fibers 15

16 (mantle and core) within a nerve may also play a role. The depolarization in myelinated fibers is saltatory. About three nodes of Ranvier need to be blocked in order to block the transmission of the action potential. The smallest nerve fibers are nonmyelinated and are blocked more readily than larger myelinated fibers. However at similar size myelinated fibers are blocked before nonmyelinated fibers. In general autonomic fibers, small nonmyelinated C fibers (mediating pain), and small myelinated A delta fibers (mediating pain and temperature) are blocked before A gamma, A β and A α fibers (postural, touch, pressure and motor information). In large nerve trunks motor fibers are usually located in the outer portion (mantle) of the bundle and are more accessible to local anesthetics. Thus motor fibers may be blocked before sensory fibers in large mixed nerves. In addition the frequencydependence of local anesthetic action favors block of small sensory fibers as they generate long action potential (5 ms) at high frequency, whereas motor fibers generate short action potentials (0.5 ms) at lower frequency. These characteristics of sensory fibers in general, and of pain fibers in particular, favor frequency-dependent block. (Figure from Morgan s Clinical Anesthesiology, 3 rd edition, 2006, with permission) Modulating local anesthetic action ph adjustment The ionized molecule of local anesthetics is the active form in the Na + channel, although it is the non-ionized fraction the one that starts the whole process by crossing the nerve membrane. The rate-limiting step in this cascade is membrane penetration of local anesthetics in its non-ionized form. Unfortunately only a small proportion of local anesthetic in solution exists in the non-ionized state. Changes in ph can theoretically reduce the onset time by increasing its proportion. At a ph of 5.0 to 5.5 the cation/base 16

17 ratio is 1000:1, at a ph of 7.4 the same ratio becomes 60:40. The limiting factor for ph adjustment is the solubility of the base form before reaching precipitation. The most lipid soluble agents like bupivacaine and ropivacaine cannot be alkalinized above a ph of 6.5 because they precipitate. DiFazio et al (Anesth Analg 1986:65; ) demonstrated a more than 50% decrease in onset of epidural anesthesia when the ph of commercially available lidocaine with epinephrine was raised from 4.5 to 7.2 by the addition of bicarbonate. Capogna et al (Reg Anesth 1995; 20: ) randomized 180 patients to study the effects of alkalinizing lidocaine, mepivacaine and bupivacaine for blocks. They concluded that alkalinization of lidocaine and bupivacaine shortens the onset of epidural; alkalinization of lidocaine shortens the onset of axillary block and alkalinization of mepivacaine shortens the onset of sciatic/femoral blocks. However, when only small changes in ph can be achieved because of the limited solubility of the base, only small decreases in onset time will occur, as when plain bupivacaine is alkalinized. It is generally believed that adding bicarbonate to speed the onset of action of local anesthetics applies more to local anesthetics solutions that have epinephrine added by the manufacturer (lower ph) rather than when fresh epinephrine is added or a plain solution is used. Chloroprocaine plus 1 ml of sodium bicarbonate for 30 ml of solution raises the ph to 6.8. Adding 1 ml of sodium bicarbonate per 10 ml of lidocaine or mepivacaine raises the ph of the solution to 7.2 and adding 0.1 ml of bicarbonate per 10 ml of bupivacaine raises the ph of the solution to 6.4 (from Mulroy s Regional anesthesia, 3 rd edition, 2002). Carbonation Another approach to shortening onset time has been the use of carbonated local anesthetic solutions. These solutions contain large amounts of carbon dioxide, which readily diffuses into the axoplasm of the nerve lowering the ph and favoring the formation of the cationic active form of the local anesthetic. Carbonated solutions are not available in the United States. LOCAL ANESTHETICS ADDITIVES Vasoconstrictors Epinephrine is the most common vasoconstrictor added to local anesthetics to prolong the anesthetic effect and to decrease absorption. Epinephrine is also used to detect intravascular injection. Without beta-blockers on board 15 µg of fentanyl produce a 30% increase in heart rate within 30 seconds. Vasoconstrictors may also improve the quality and density of the block especially with spinal and epidural anesthesia. This has been demonstrated with tetracaine, lidocaine and bupivacaine. The mechanism is unclear. Epinephrine may simply increase the amount of local anesthetic available by reducing absorption. It could also have some local anesthetic effect by means of its α 2-agonist actions. Subarachnoid epinephrine also delays voiding and discharge readiness. The prolongation of effect in peripheral nerve blocks can be 30 to 60% depending on site of injection and type of local anesthetics (more vascular sites like intercostal see more effect, and intermediate agents like lidocaine benefit more). Peripherally epinephrine does not have any significant alpha-2 effect. 17

18 Spinal anesthesia is more prolonged with less lipid soluble agents like lidocaine, mepivacaine (20-30%) but the exception is tetracaine that gets the largest prolongation of up to 60% in lumbar dermatomes. The intrathecal dose of epinephrine is usually 200 µg but doses as small as 50µg can be sufficient. In the epidural space usually the dose is 5 µg/ml. Epinephrine other than intrathecally is absorbed systemically and may produce adverse cardiovascular effects. In small doses the beta-adrenergic effects predominate with increased cardiac output and heart rate. Dose larger than 0.25 mg (250 µg) may be associated with arrhythmias or other undesirable cardiac effects. Lately concerns have been raised about potential peripheral nerve ischemia caused by epinephrine acting on epineural vessels and vaso nervorum. This potential risk has to be balanced against lower risk of systemic toxicity, ability to detect intravascular injection and prolongation of action. According to Neal (Reg Anesth Pain Med 2003;28: ) adding 5 ug/ml (1:200,000 dilution) prolongs the duration of lidocaine for peripheral nerve blocks from 186 min to 264 min. Adding only 2.5 ug/ml (1:400,000 dilution) prolongs the block to 240 min (almost the same prolongation) without apparent effect on nerve blood flow. Patients with micro angiopathy (e.g., diabetics) who could be at increase risk for neural ischemia secondary to vasoconstriction potentially could benefit from the use of more diluted epinephrine. Adding only 1:400,000 epinephrine to our local anesthetic solutions for nerve blocks has become the standard in our practice. Intrathecal epinephrine does not lead to cord ischemia because it does not decrease spinal cord blood flow although it decreases epidural blood flow (Kosody R, et al. Can Anaesth Soc J; 31: 503-8, 1984). In fact spinal cord ischemia due to epinephrine is improbable because the cord vessels are autoregulated and show very minimal response to endogenous or exogenous vasoactive agents (Neal JM in: Regional Anesthesia, The Requisites. Elsevier Mosby, Philadelphia 2004, pp25-31) Although epinephrine-containing local anesthetics are usually contraindicated in areas of terminal circulation (e.g., digits) this recommendation is not based on hard evidence. Anecdotal use of epinephrine-containing solutions in these areas is cited in the literature. Lalonde et al in a multicenter study published 3,110 consecutive cases of use of epinephrine in the fingers and hand from The authors (surgeons) defined low dose epinephrine as 1:100,000 and they reported no instance of digital tissue loss (J Hand Surg 2005; 30: ). We do not recommend it. Dilution/concentration issues 1:1 dilution means 1 g solute in 1 ml of solvent, so a dilution of: o 1:1,000 means 1 g in 1,000 ml or 1 mg/ml or 1,000 µg/ml o 1:100,000 equals 0.01mg/mL or 10 µg/ml o 1:200,000 equals mg/ml or 5 µg/ml o 1:400,000 equals mg/ml or 2.5 µg/ml Opioids Neuraxial use: The addition of opioids to local anesthetics has a synergistic effect both in anesthesia and postoperative analgesia (especially visceral pain). They block pain pathways without significantly affecting motor or sympathetic fibers. 18

19 The hydrophilic opioid morphine can be used in doses of mg spinal and 1-3 mg epidural. It has a slow onset of 45 min, analgesic action lasting h, reaching the brainstem and 4 th ventricle slowly (delayed respiratory depression). Delayed respiratory depression (8-10 h) is a risk with all neuraxial opioids but is more frequently seen with hydrophilic drugs like morphine, and in susceptible populations like the elderly and debilitated. Neuraxial morphine is also associated with higher incidence (40-50%) of nausea and vomiting than systemic opioids, pruritus in 60-80% (20% severe), and delayed voiding. It is not suitable for outpatients. Short-acting opioids such as fentanyl and sufentanil added to spinal anesthetics also intensify the block and prolong the duration of anesthesia beyond the duration of local anesthetics. Respiratory depression with these agents is rare and usually early (within 4 h). Sufentanil spinal can be used in doses of µg. Fentanyl spinal is used in doses of µg and µg epidural. Onset occurs at 5-15 min, peak effect at min and duration of 1-3 h. Hypotension, pruritus, nausea and vomiting are some common side effects. Extended-release epidural morphine (DepoDur) is a new liposomal formulation designed for epidural use providing 48 h of pain relief. DepoDur approved in 2004 is supplied in a 2 ml vial containing 10 mg/ml dose in sterile saline. It is only approved as a single lumbar epidural dose prior to surgery (or after clamping of the umbilical cord during C-section). The recommended dose is 10 mg for C-section, mg for lower abdominal surgery and 15 mg for major orthopedic surgery of the lower extremities. Respiratory depression is dose-related. The most common adverse events reported during clinical trials were decreased oxygen saturation, hypotension, urinary retention, nausea and vomiting, constipation and pruritus. Peripheral nerve blocks: The usefulness of opioids in peripheral nerve blocks is mostly unsupported by the evidence. Opioids have been shown useful when injected in the intraarticular space. Clonidine Alpha-2 agonists have central (sedation, analgesia, bradycardia) and peripheral effects (vasoconstriction/vasodilation with net hypotension, anti shivering, diuresis). The site for sedative action is the locus ceruleus of the brain stem while the principal site for analgesia seems to be the spinal cord. The main alpha-2 effect on the heart is decreased tachycardia by blocking cardioacelerator fibers and bradycardia through a vagomimetic effect. In the periphery they produce both vasodilation via sympatholysis and vasoconstriction through receptors on smooth muscle. The cause for their antishivering and diuretic effects are yet to be established. Side effects (sedation, hypotension, bradycardia) limit their use. Small doses (50-75 µg) have shown to significantly prolong analgesia in spinal, epidural, IV regional, and peripheral nerve blocks both when injected with the LA and when given orally. Injected intrathecally they also can delay voiding and can produce orthostasis. Side effects do not occur often at doses below 1.5 µg/kg or a total dose less than 150 µg. 19

20 Iskandar et al in France in 2001 showed that adding 50 µg of clonidine to selected nerves (median and musculocutaneous) prolongs mepivacaine sensory anesthesia in those nerves territories after a mid-humeral block by 50% compared to placebo without prolonging motor effect. Because the prolongation was observed only in the nerves that received clonidine they postulated that the effect must be peripheral and not central through absorption. Dexmedetomidine It is a more selective alpha-2 agonist agent with an alpha-2: alpha-1 receptor ratio of 1,600:1, seven times greater than that of clonidine. Its elimination half-life is only 2 h compared to more than 8 h for clonidine. Dexmedetomidine may offer extended analgesia with lesser side effects. Currently it is approved only for sedation in the ICU. Neostigmine It is an acetylcholinesterase inhibitor that prevents the breakdown of acetylcholine promoting its accumulation. Acetylcholine is an endogenous spinal neurotransmitter that induces analgesia. Neostigmine does not cause neural blockade nor have any action on opioid receptors. Spencer Liu et al in 1999 (Anesthesiology 1999; 90:710-17) studied the effects of different doses of neostigmine added to bupivacaine spinal. They reported that 50 µg of neostigmine increased sensory and motor anesthesia but also delayed discharge time and was accompanied by 67% nausea and up to 50% vomiting. Lower doses did not show analgesic effect but still had significant rates of side effects (nausea and vomiting). N-methyl-D-aspartate (NMDA) receptor antagonists Activation of NMDA receptors makes the neurons of the spinal cord more responsive to all types of input including pain stimuli (central sensitization). NMDA receptor antagonists like ketamine have shown analgesic activity. In fact in IV regional 0.1 mg/kg of ketamine is superior to clonidine (1 µg/kg) in preventing tourniquet pain. Errando in Spain showed that commercially available ketamine containing benzethonium chloride is toxic in swine (Reg Anesth Pain Med 1999; 24:146-52). Preservative-free solutions of ketamine have proven safe. Hyaluronidase It breaks down collagen bonds potentially facilitating the spread of local anesthetic through tissue planes. The evidence shows however that at least in the epidural space it can decrease the quality of anesthesia. Its use seems limited to retrobulbar blocks. Dextran Dextran and other high-molecular-weight compounds have been advocated to increase the duration of local anesthetics. The evidence is lacking. METABOLISM OF LOCAL ANESTHETICS Ester local anesthetics They are hydrolyzed at the ester linkage by plasma pseudocholinesterase, the same enzyme that hydrolyses acetylcholine and succinylcholine. The hydrolysis of 2-20

21 chloroprocaine is about four times faster than procaine, which in turn is hydrolyzed about four times faster than tetracaine. In individuals with atypical plasma pseudocholinesterase the half-life of these drugs is prolonged and potentially could lead to plasma accumulation. Cerebrospinal fluid does not contain esterase enzymes so if an ester is used for spinal anesthesia (e.g., tetracaine) its termination of action depends on blood absorption. The hydrolysis of all ester local anesthetics leads to the formation of paraaminobenzoic acid (PABA), which is associated with a low potential for allergic reactions. Allergic reactions may also develop from the use of multiple dose vials of amide local anesthetics that contain methylparaben (PABA derivative) as a preservative. As opposed to other ester type anesthetics, cocaine is partially metabolized in the liver and partially excreted unchanged in the urine. Amide local anesthetics They are transported into the liver before their biotransformation. The two major factors controlling the clearance of amide local anesthetics by the liver are hepatic blood flow and hepatic function. The metabolism of local anesthetics as well as that of many other drugs occurs in the liver by the cytochrome P-450 enzyme system. Because of the liver large metabolic capacity it is unlikely that drug interaction would affect the metabolism of local anesthetics. The rate of metabolism is agent specific (prilocaine > lidocaine > mepivacaine > ropivacaine > bupivacaine). The metabolism of amide local anesthetics is relatively fast. Elimination half-life for lidocaine is h. Drugs such as general anesthetics, norepinephrine, cimetidine, propranolol and calcium channel blockers can decrease hepatic blood flow and potentially increase the elimination half-life of amides. Similarly, decreases in hepatic function caused by a lowering of body temperature, immaturity of the hepatic enzyme system in the fetus, or liver damage (e.g., cirrhosis) can lead to decreased rate of hepatic metabolism of the amides. Renal clearance of unchanged local anesthetic is a minor route of elimination (e.g., lidocaine is only 3% to 5% recovered unchanged in the urine of adults while bupivacaine is 10% to 16%). The dibucaine number People with atypical plasma pseudocholinesterase exhibit prolonged recovery after a dose of succinylcholine or mivacurium. Dibucaine is an amide local anesthetic that helps to identify those patients. Dibucaine binds strongly to normal plasma pseudocholinesterase inhibiting its action. This inhibition is reported as a number from representing the percentage of normal enzyme inhibition, the larger the number the better. A number of 80 or higher means that dibucaine is able to inhibit at least 80% of the enzyme and that the patient is normal homozygous. A dose of succinylcholine will last 4-6 min. A dibucaine number of 50 means that the patient is heterozygous and that the effect of succinylcholine will be prolonged to up to 30 min. A number of 20 is related to the homozygous atypical enzyme and the effect of succinylcholine could be expected to last up to 6 h (incidence 1:3,300). 21

22 LOCAL ANESTHETIC TOXICITY Systemic local anesthesia toxicity is related to plasma levels which depend on: 1. Total dose 2. Net absorption, which depends on: vasoactivity of the drug, site vascularity and use of a vasoconstrictor 3. Biotransformation and elimination of the drug from the circulation Both CNS and CV effects are poorly correlated with arterial drug concentrations and better correlated with regional venous drainage. Lung uptake reduces the drug concentration by 40% and slower injection (3 min compared to 1 min) achieves similar decreases (Reg Anesth Pain Med 2005; 30: ). Peak local anesthetic blood levels are directly related to the dose administered at any given site. However the vascularity of the site at similar doses is very important in determining different plasma levels: endotracheal > intercostal > caudal > epidural > plexus blocks > sciatic/femoral. Generally the administration of a 100-mg dose of lidocaine in the epidural or caudal space results in approximately a 1 µg/ml peak blood level in an average adult. The same dose injected into less vascular areas (e.g., brachial plexus axillary approach or subcutaneous infiltration) produces a peak blood level of app 0.5 µg/ml. The same dose injected intercostal produces a 1.5 µg/ml plasma level. Peak blood levels may also be affected by the rate of biotransformation and elimination. In general this is the case only for very actively metabolized drugs such as 2- chloroprocaine, which has a plasma half-life of about seconds. For amide local anesthetics like lidocaine peak plasma levels after regional anesthesia primarily result from absorption and in general occur within 1 h (please see difference with tumescent anesthesia). Rodriguez et al (Eur J Anaesthesiol 2001; 18: 171-6) studied 10 end-stage renal disease patients coming for A-V fistula. The patients received an axillary block with a total of 650 mg of plain mepivacaine. Plasma levels were studied during 150 min. Peak levels of 8.28 ( ) µg/ml were obtained within 60 min and decreased steadily thereafter. Patients did not exhibit signs of toxicity despite high plasma levels (more than 5 µg/ml). This is in contrast with a case report by Tanoubi et al (Ann Fr Anesthe Reanim 2006; 25: 33-5) where an end-stage renal patient for A-V fistula received an axillary block with 375 mg (25 ml) of 1.5% mepivacaine and the patient presented with dysarthria, mental confusion and loss of consciousness without convulsions or arrhythmia. Mepivacaine plasma level at the time of symptoms was 5.1 µg/ml. Tumescent (diluted) anesthesia for liposuction The use of highly diluted lidocaine concentrations (0.1% or less) plus epinephrine (usually 1 mg per liter or 1:1,000,000) allows for a painless and bloodless liposuction procedures. Lidocaine bounds to tissue proteins in this subdermal drug reservoir (22) from where it is subsequently slowly released into the systemic circulation. Diluted lidocaine along with epinephrine-induced vasoconstriction make systemic uptake so slow as to match the liver maximum lidocaine clearance capacity of 250 mg/h. Thus the blood level remains below 5 µg/ml toxic threshold, despite the administration of many times (e.g., 35 mg/kg) the conventional upper dose limit of undiluted full strength lidocaine (de Jong 2002). 22

23 Peak plasma levels of lidocaine using tumescent technique occur between 5-17 hours compared to less than 1 h for common infiltration. Central nervous system toxicity Toxic plasma levels are usually produced by inadvertent intravascular injection. It can also result from the slow absorption following peripheral injection. A sequence of symptoms can include: Numbness of the tongue, lightheadedness, tinnitus, restlessness, tachycardia, convulsions and respiratory arrest. Cardiovascular system toxicity The cardiovascular manifestations usually follow the CNS effects (therapeutic index). The exception is bupivacaine, which can produce cardiac toxicity at sub convulsant concentrations. Rhythm and conduction are rarely affected by lidocaine, mepivacaine and tetracaine but bupivacaine and etidocaine can produce ventricular arrhythmias. EKG shows a prolongation of PR and widening of the QRS Higher incidence in pregnancy CV toxicity is increased under hypoxia and acidosis. Toxic plasma concentration thresholds Lidocaine 5 µg/ml; mepivacaine 5 µg/ml; bupivacaine 1.5 µg/ml; ropivacaine 4 µg/ml Management of systemic toxicity The best treatment for toxic reactions is prevention. When local anestheticinduced seizures occur, hypoxia, hypercarbia and acidosis develop rapidly. ABC (Airway, Breathing and Circulation) is the mainstay of treatment. Administration of O 2 by mask or ventilation support by bag and mask is often all that is necessary to treat seizures. If seizures interfere with ventilation benzodiazepines, propofol or thiopental can be used. The use of succinylcholine effectively facilitates ventilation and by abolishing muscular activity decreases the severity of acidosis. However neuronal seizure activity is not inhibited and thus cerebral metabolism and oxygen requirements remain increased. Little information is available regarding the treatment of cardiovascular toxicity of LA in humans. Animal data suggest that 1) high doses of epinephrine (1 mg IV every 3-5 minutes) may be necessary to support heart rate and blood pressure although vasopressin (40 U IV, single dose, one time only) is more frequently used now before epinephrine; 2) atropine may be useful for bradycardia; 3) DC cardioversion is often successful; and 4) ventricular arrhythmias are probably better treated with amiodarone than with lidocaine. Amiodarone is used as for ACLS, 150 mg over 10 min, followed by 1 mg/min for 6 hrs then 0.5 mg/min. Supplementary infusion of 150 mg as necessary up to 2 g. For pulseless VT or VF, initial administration is 300 mg rapid infusion in ml of saline or dextrose in water. Bupivacaine toxicity and the use of lipid emulsion to treat it Bupivacaine cardiac toxicity was highlighted in an editorial report by Albright in 1979 on refractory cardiac arrests on several patients (Anesthesiology 1979; 51:285-7). In 23

24 2003 Weinberg and colleagues at the University of Illinois published (Reg Anesth Pain Med 2003; 28: ) an interesting paper describing the use of a 20% lipid emulsion in combination with cardiac massage to successfully return normal hemodynamics to 9 out 9 dogs after asystole brought by a bolus injection of 10 mg/kg of bupivacaine. They recommend treating bupivacaine-associated cardiac arrest by injecting a 1 ml/kg bolus of 20% lipid emulsion (such as intralipid) followed ay an infusion of 0.25 ml/kg/min for 10 min while continuing basic life support. The bolus can be repeated every 5 min up to three times as needed. The maximum dose of 20% lipid emulsion is not known but the authors suggest that more than 8 ml/kg would not likely be needed, nor successful if lower doses do not work. This protocol will deliver a significant volume load to the patient. The paper was accompanied by an editorial written By Groban and Butterworth from Wake Forest, in Winston-Salem, North Carolina. They believe that the most likely mechanism of action of lipid emulsion is that in some way the lipid is serving to more rapidly remove LA molecules from whatever binding site serves to produce the cardiovascular depression that has come to be known as bupivacaine toxicity. ACLS protocols must be followed with prompt defibrillation and use of pressors like epinephrine or vasopressin to support coronary perfusion if necessary. Amiodarone should be favored over lidocaine to treat arrhythmias and initiate the lipid emulsion at the earliest sign of severe local anesthetic-induced cardiac toxicity. More recently in 2006 Rosenblatt et al (Anesthesiology 2006; 105: 217-8) published a case report of successful use of 20% lipid emulsion (Intralipid, Baxter Pharmaceuticals) on a 58-year old male who developed cardiac arrest presumably linked to bupivacaine for interscalene block. After 20 min of cardiac compressions and patient in asystole 100 ml of intralipid IV was given resulting in an immediate return of patient s rhythm. This dose is higher than the recommended 1 ml/kg. A continuous infusion of intralipid was given at 0.5 ml/kg/min for 2 h. The patient was extubated 2.5 after hours after the episode and was neurologically intact. In an accompanying editorial Weinberg suggest having 20% lipid emulsion available in all sites where local anesthetics are used. In summary: 1. Evidence is accumulating on the beneficial effect of a 20% lipid emulsion to treat bupivacaine-related cardiac toxicity. 2. Propofol has the same vehicle than intralipid but at only half the concentration (10%). Giving propofol probably will not provide enough lipids, but instead it will produce a negative inotropic effect due to the presence of the active ingredient di-isopropylphenol (anesthetic action) exacerbating cardiac depression. Thus propofol is not indicated to treat local anesthetic-induced cardiac toxicity. The question remains as to whether propofol may be a better agent for sedation in cases where big volumes of LA are going to be used. In another interesting study by Mayr et al, out of Innsbruck, Austria and published in Anesth Analg 2004;98:1426-3, the authors induced cardiac arrest in 28 pigs after administering 5 mg/kg of a 0.5% bupivacaine solution and stopping ventilation until asystole occurred. CPR was initiated after 1 min of cardiac arrest. After 2 min the 24

25 animals received every 5 min either epinephrine alone; vasopressin alone; epinephrine plus vasopressin or placebo IV. In the vasopressin/epinephrine group all pigs survived and in the placebo group all pigs died. In the vasopressin alone 5 of 7 survived and in the epinephrine group 4 of 7 survived. Maximum dose Regional anesthesiologists perform peripheral nerve blocks with an amount of local anesthetics that usually exceeds the maximum recommended doses. The common recommendations for maximum doses as suggested by the literature are not evidence based (14) and have proven to be poor approximation of safety (15). It is known that peak plasma levels do not correlate with patient size or body weight. Many practitioners have called to review these guidelines to better reflect the reality of clinical practice. The American Society of Regional Anesthesia convened a Conference in Local Anesthetic Toxicity with a panel of experts in 2001 to discuss the subject. Many papers related to that conference have been published. In a review article by Rosenberg et al (14) the authors propose that the safe ranges should be block specific and related to patient s age (e.g., epidural), organ dysfunction (especially for repeated doses) and pregnancy. They suggest also adding epinephrine 2.5 to 5 µg/ml when not contraindicated. The fact is that most of the systemic toxicity occurs with unintentional direct intravascular injection (16). Methemoglobinemia Normal hemoglobin contains an iron molecule in the reduced or ferrous form (Fe 2+ ). Hemoglobin can transport oxygen only when the iron atom is in its ferrous form. When hemoglobin is oxidized, the iron molecule is converted into the ferric state (Fe 3+ ) or methemoglobin. Methemoglobin lacks the electron that is needed to form a bond with oxygen and, thus, it is incapable of oxygen transport. Because red blood cells are continuously exposed to various oxidant stresses, blood normally contains approximately 1% methemoglobin levels. Prilocaine and benzocaine can oxidize the ferrous form of the hemoglobin to the ferric form, creating methemoglobin. It is more frequently seen with nitrates as nitroglycerin. When MetHb exceeds 4 g/dl cyanosis can occur. Prilocaine doses of more than 600 mg are needed to produce clinically significant methemoglobinemia. Depending on the degree methemoglobinemia can lead to tissue hypoxia. The oxyhb curve shifts to the left (P50 < 27 mmhg). MetHb has a larger absorbance than Hb and 0 2 Hb at 940 nm but simulates Hb at 660 nm. In the presence of high MetHb concentrations the SaO 2 falsely approaches 85% independent of the actual arterial oxygenation. Diagnosis needs clinical suspicion and blood gases. Methemoglobinemia is easily treated by the administration of methylene blue (1-2mg/kg of a 1% solution over 5 min) or less successfully with ascorbic acid (2 mg/kg). Allergy True allergy (type I or IgE mediated) to local anesthetics is rare and presents within minutes after the exposure. It is relatively more frequent with esters, which are metabolized to para-amino-benzoic acid (PABA). PABA is frequently used in the pharmaceutical and cosmetic industries. Allergy to amide local anesthetics is exceedingly 25

26 rare. There is no cross allergy between esters and amides. However use of methylparaben as a preservative in multidose vials can elicit allergy in patients allergic to PABA. Delayed hypersensitivity reactions (type IV) are T-cell mediated and present 24 to 48 h after exposure. There are few cases in the literature of delayed hypersensitivity to lidocaine but recent reports suggest it may be more frequent than previously reported. The North American Contact Dermatitis Group found that 0.7 % of patients who were patch tested in demonstrated delayed allergy to lidocaine (ASRA News, February 2006). Eutectic mixture of local anesthetics (EMLA) Eutectic means easily melted according to Morgan. EMLA cream is a 1:1 mixture of 5% lidocaine and 5% prilocaine. One gram of EMLA contains 25 mg of lidocaine, 25 mg of prilocaine, an emulsifier, a thickener and distilled water. EMLA is a liquid at room temperature containing up to 80% concentration of the uncharged base form of local anesthetic, which confers better dermal penetration. One or 2 grams of EMLA cream are applied per 10 cm 2 of skin and covered with an occlusive dressing (maximum application area 2000 cm 2 or 100 cm 2 in children less than 10 kg). Onset of anesthesia occurs between 45 to 60 minutes. Its main use is in children. Drug interactions Local anesthetics potentiate the effects of non-depolarizing muscle relaxants. Simultaneous administration of succinylcholine and ester local anesthetics, both metabolized by pseudocholinesterases, may potentiate the effect of each other. Cimetidine and propranolol decrease hepatic blood flow and amide local anesthetic clearance increasing the potential for systemic toxicity. Opioids and alpha-2 adrenergic agonists potentiate the effects of local anesthetics and vice versa. SPECIFIC AGENTS 1. Procaine: Ester, pka 8.9, intermediate onset, low potency, short duration. Very short half-life (20 sec), protein binding 5%. It provides a short-duration spinal (potential benefit on outpatients) Chloroprocaine: Ester, pka 9.3, very fast onset despite high pka (ability to use higher concentrations could be the reason). Very short half-life (30 sec). Negligible protein binding. Short duration (it has 30 minutes 2-segment regression in epidural). The original preparation contained sodium metabisulfite, which was associated with serious neurological deficits after massive intrathecal injection planned for epidural were given intrathecally. A second preservative ethylenediamine tetra-acetic acid (EDTA) was associated with severe muscle spasm after epidural in ambulatory patients. EDTA chelates ionized calcium and its action may have been on paraspinal muscles. The present solution is prepared without preservative and no back spasms have been reported. 3. Tetracaine: ester, pka 8.6, slow onset, high potency, short plasma half-life (2.5 to 4 min) and long duration of action. It is 85% protein bound. Early experience with this product at high doses resulted in CNS toxicity giving it a bad reputation, which is mostly undeserved. We still use it occasionally as 26

27 lyophilized crystals dissolved in liquid mepivacaine for a concentration of 0.2% tetracaine to prolong duration of peripheral nerve blocks to 4-6 h of surgical anesthesia. Tetracaine also is the drug that most benefit from adding epinephrine to spinal anesthesia (up to 60% in the lumbar dermatomes). 4. Cocaine: ester, pka 8.6, slow onset, short duration. It produces vasoconstriction while most of the LA with the exception of ropivacaine produce some degree of vasodilation. It interferes with the reuptake of cathecolamines resulting in hypertension, tachycardia, arrhythmia and myocardial ischemia. It is used mainly for topical anesthesia of the nose. Doses below 100 mg are usually safe. Cocaine can potentiate cathecolamine-induced arrhythmias by halothane, theophylline or antidepressants. Cocaine can induce coronary vasospasm and potential myocardial ischemia without the need for coronary artery disease. Mixtures of lidocaine and phenylephrine are safer alternatives. Up to 9% is eliminated unchanged in the urine, especially acid urine. At the end of 4 h most of the drug is eliminated from the plasma but some metabolites may be identified up to 144 h after administration (Ellenhom and Barceloux, 1988). 5. Benzocaine: ester, pka 3.5, slow onset, short duration and the only LA with a secondary amine structure that limits its ability to pass through membranes. It is used as a topical anesthetic. Doses higher than 300 mg can induce methemoglobinemia. 6. Lidocaine: amide, pka 7.8, intermediate onset and duration, elimination half-life min. It is 65% protein bound; it is versatile (topical, infiltration, IV regional, neuraxial, antiarrhythmic) and widely used. Spinal use is associated with around 30% of TNS especially with lithotomy position, knee arthroscopy and obesity. Lowering the concentration does not eliminate the problem with doses larger than 40 mg. Doses of mg highly reduce the incidence of TNS. 7. Mepivacaine: amide, pka 7.6, intermediate onset and duration. Elimination halflife is 2-3 h in adults and 8-9 in neonates. It is 75% protein bound and seems to produce less vasodilation than lidocaine. It has been used in spinal anesthesia. It has lower (but not zero) incidence of TNS. It is our most common agent for peripheral nerve blocks where a 1.5% concentration provides a short onset and dense surgical anesthesia lasting 2-3 h plain and 3-4 h with 1:400,000 epinephrine. Prolonged postoperative analgesia as with all the other LA is negligible after single-shot blocks. 8. Bupivacaine: amide, pka 8.1, high potency, slow onset, long duration. Elimination half-life h in adults and around 8 h in neonates. It is 95% protein bound. Lower concentrations (0.25% and less) produce analgesia with increased motor sparing (desirable in outpatients). Commercial bupivacaine is a 50:50 racemic mixture of the S and R enantiomers. Cardiac arrest associated with bupivacaine is difficult to treat possibly due to high protein binding and high lipid solubility (please see toxicity). 9. Ropivacaine: amide, pka 8.2, onset and duration similar to bupivacaine with slight lesser potency. It is 94% protein bound. Elimination half-life 1-3 h in adults. Like bupivacaine it is chemically related to mepivacaine, but as opposed to most local anesthetics it is supplied as the pure S enantiomer of the drug. At lower concentrations (less than 0.5%) there may be a greater selectivity for sensory than 27

28 motor blockade than bupivacaine. The S enantiomer is associated with less cardiac toxicity, intermediate between that of lidocaine and bupivacaine. It is a weak vasoconstrictor (only one other than cocaine). 10. Levobupivacaine: amide, S enantiomer of bupivacaine, very similar to ropivacaine. 28

29 References 1. Raj P; Textbook of Regional Anesthesia, 2002 chapter Longnecker DE et al. Principles and Practice of Anesthesiology, chapters Cousins et al. Neural blockade, 3 rd edition 1998 chapters Morgan s Clinical Anesthesiology, 4th edition, Mulroy s Regional Anesthesia, 3 rd edition, Barash s Clinical Anesthesia, 5 th edition, 2006, chapter Anesth Clinics of North America 2000:18:2 8. DiFazio et al Anesth Analg 1986:65; Hilgier. Reg Anesth 1985:10; Weinberg GL et al. Lipid emulsion infusion rescues dogs from bupivacaineinduced cardiac toxicity. Reg Anesth Pain Med 2003; 28: Mayr et al. A comparison of epinephrine and vasopressin in a porcine model of cardiac arrest after rapid intravenous injection of bupivacaine. Anesth Analg 2004; 98: Neal JM. Effects of epinephrine in local anesthetics on the central and peripheral nervous systems: Neurotoxicity and neural blood flow. Reg Anesth Pain Med 2003; 28: Enneking FK, et al. Lower-extremity peripheral nerve blockade: Essentials of our current understanding. Reg Anesth Pain Med 2005; 30: Rosenberg PH, Veering VT, Urmey WF. Maximum recommended doses of local anesthetics: A multifactorial concept. Reg Anesth Pain Med 2004; 29: Mulroy M. Local anesthetics: Helpful science, but don t forget the basic clinical steps (editorial). Reg Anesth Pain Med 2005; 30: Mather L, Copeland S, Ladd L. Acute toxicity of local anesthetics: underlying pharmacokinetics and pharmacodynamics concepts (A review article). Reg Anesth Pain Med 2005; 30: One hundred years later, I can still make your heart stop and your legs weak: the relationship between regional anesthesia and local anesthetic toxicity. Reg Anesth Pain Med 2002; 27(6): Systemic toxicity and cardiotoxicity from local anesthetics: Incidence and preventative measures. Reg Anesth Pain Med 2002; 27(6): Local anesthetic toxicity, does product labeling reflect actual risk? Reg Anesth Pain Med 2002; 27(6): Current concepts in resuscitation of patients with local anesthetic cardiac toxicity. Reg Anesth Pain Med 2002; 27(6): Myer Leonard. Carl Koller: Mankind s greatest benefactor? The story of local anesthesia. J Dent Res 1998; 77: De Jong R. Tumescent anesthesia: lidocaine dosing dichotomy. Int J Cosmetic Surg 2002; 4: Nordstrom H, Stange K. Plasma lidocaine levels and risks after liposuction with tumescent anaesthesia. Acta Anaesthesiol Scand 2005; 49: Rosenblatt M et al. Successful use of a 20% lipid emulsion Anesthesiology 2006; 105:

30 25. Rodriguez J et al. High doses of mepivacaine for brachial plexus block in patients with end-stage chronic renal failure. A pilot study. Eur J Anaesthesiol 2001; 18: Kamibayashi et al. Clinical uses of α 2 -adrenergic agonists. Anesthesiology 2000; 93: Tanoubi I et al. Systemic toxicity with mepivacaine following axillary block in a patient with terminal kidney failure. Ann Fr Anesth Reanim 2006; 25:

31 CHAPTER 3 NEURAXIAL ANESTHESIA Spinal anesthesia Anatomy...32 Cerebrospinal fluid...33 Site of action and indications...34 Baricity.34 Local anesthetic distribution 35 Techniques (median, paramedian, Taylor s) 35 Anesthesia duration. 36 Side effects and complications.36 Physiological effects.37 Postdural puncture headache 38 Transient neurological symptoms.39 Cauda equina syndrome...40 Back pain.40 Spinal in the outpatient.40 Intrathecal adjuncts...41 Epidural Anesthesia Anatomy...42 Blockade characteristics...42 Spread of local anesthetics...42 Techniques 42 Type of needles and catheters..43 Test dose...43 Activating an epidural..43 Termination of action...43 References 44 31

32 SPINAL ANESTHESIA It is one of the easiest and most reliable techniques of regional anesthesia. Because of the very small doses of local anesthetics involved, these drugs have not direct systemic effects. In 1885 James Corning, an American neurologist, was the first person to use cocaine intrathecally to treat some neurological conditions. Augustus Bier, a German surgeon, was the first person to use intrathecal cocaine to produce surgical anesthesia. In a classic paper published in 1899 he described the performance of spinal anesthesia on himself and on his assistant Hildebrandt. These became also the first two described cases of post dural puncture headaches. Anatomy The spinal canal has a protective sheath composed of three layers. From the outside to the inside they are: duramater, arachnoid and piamater. The potential space between the dura and arachnoid is called subdural space. The cerebrospinal fluid (CSF) flows between the arachnoid and piamater in the space called subarachnoid space. The spinal cord begins superiorly at the foramen magnum as a continuation of the medulla oblongata. It terminates inferiorly at the conus medullaris, which in the adult corresponds to the level of the lower border of L1 and in the young child to the upper border of L3. From this end a prolongation of the piamater called the filum terminale attaches the spinal cord to the back of the coccyx. The dural sac itself ends at the level of the second sacral vertebra. The spinal cord is composed of a core of gray matter surrounded by white matter. The gray matter on cross section has an H shape with anterior (motor) and posterior (sensory) horns. The white matter is described as having anterior, lateral and posterior white columns. There are 31 pairs of spinal nerves; each one possesses a ventral or motor root and a dorsal or sensory root. The dorsal root has the dorsal root ganglion. Because in the adult the spinal cord is shorter relatively to the vertebral column the spinal nerves descend a variable distance in the spinal canal before exiting through the intervertebral foramen. The most distal lumbar and sacral nerves travel the longest distance inside the spinal canal forming what is known as the cauda equina. As the spinal nerve pierces the dura sac, it draws with it a dural sleeve. The spinal nerves exit through the intervebral foramen, formed between two vertebrae. There are 8 cervical nerves, the first cervical nerve exits through the occipital bone and C1, the 8 th cervical nerve exits between C7 and T1. Distal to T1 each spinal nerve exits below the corresponding vertebra. The vertebral column has a series of curvatures in the anteroposterior plane. The cervical and lumbar curvatures have an anterior convexity (lordosis) and the thoracic and sacral have posterior convexity (xiphosis). These curvatures play a role in the spread of hyperbaric solution as we will review later. 32

33 The blood supply to the spinal cord comes from one anterior spinal artery and two posterior spinal arteries. These arteries anastomose to form longitudinal vessels reinforced by segmental arteries that enter the vertebral canal trough the intervertebral foramina. The anterior two thirds of the spinal cord are supplied by the anterior spinal artery reinforced in the neck by branches of the vertebral artery. (Figure from Cousins s Neural Blockade, 3 rd edition, 1998, with permission) In the thoracic region the anterior spinal artery receives only a few radicular arteries from the aorta. In the lumbar region a large branch called radicularis magna or artery of Adamkiewicz reinforces the anterior spinal artery. It arises 78% of the times on the left side (risk of ischemia to the lumbar cord if damaged during retroperitoneal dissections like surgery on the distal aorta). This large branch typically enters the spinal canal through a single intervertebral foramen between T8 and L3. A case of transient paraplegia after neurolytic celiac plexus block on a pancreatic cancer patient was published in 1995 (4). The proposed mechanism was reversible arterial spasm post injection of ethanol solution. The spinal needle crosses the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, duramater and arachnoid before reaching the subarachnoid space. The space between the ligamentum flavum and duramater is the epidural space. Cerebrospinal fluid It is primarily formed in the choroids plexus of the cerebral ventricles. The CSF flows from the lateral ventricles to the third and fourth ventricles and to the cisterna magna. It flows then around the brain and spinal cord within the subarachnoid space. The CSF is absorbed into the venous system of the brain by the villi in the arachnoid membrane. CSF is formed and reabsorved at a rate of ml/min. The CSF volume in the brain is between ml. The volume of CSF below T12, where most of the spinal anesthetics are performed is, according to Hogan and collaborators (3), widely variable among individuals ranging from ml. CSF 33

34 volume is decreased with increased abdominal pressure like the one accompanying pregnancy and obesity. This effect may produce more extensive neuraxial blockade. Composition of cerebrospinal fluid and serum in humans CSF Serum Sodium (meq/l) Potassium (meq/l) Calcium (meq/l) Magnesium (meq/l) Chloride (meq/l) Bicarbonate (meq/l) Glucose mg/100ml) Protein (mg/100ml) ph Osmolality (mosm/kg H 2 O) Site of action The nerve root is the main site of action for both spinal and epidural anesthesia. In spinal anesthesia the concentration of local anesthetic in CSF is thought to have minimal effect on the spinal cord itself. Indications Abdominal and lower extremity procedures are the most common. It has been used for lumbar spine surgery. Saddle blocks are frequently used for rectal surgery. Baricity It is the result of dividing density of the local anesthetic solution by that of the CSF. The density of CSF has a mean value of If the baricity is 1.0 it is by definition isobaric; if greater than 1 it is hyperbaric and if less than 1 it is hypobaric. 1. Hypobaric solutions Tetracaine is the LA most frequently used for hypobaric spinal anesthesia. Solutions of 0.1% to 0.33% tetracaine in water are reliably hypobaric in all patients. The most common uses are for rectal procedures in jackknife position and for hip surgery injecting in lateral position with the surgical side up. 2. Isobaric solutions Tetracaine and plain bupivacaine diluted with CSF make good isobaric solutions. These solutions stay very close to the point of injection. 3. Hyperbaric solutions The easiest, safest and most widely used way of providing spinal anesthesia. The solution is rendered hyperbaric by adding glucose. Gravity and patient s position determines the spread. In supine position L3 and T6 are the highest points of the spine. 34

35 Distribution of local anesthetics in the spinal fluid Major factors Dosage, rather than volume or concentration Baricity Position of patient (except isobaric solutions) Minor factors Level of injection Increased abdominal pressure (obesity and pregnancy) Patient height (only at extremes) Coughing Direction of needle bevel can affect spread of isobaric preparations. The bevel should be directed toward the desired region. No effect Addition of vasoconstrictors Barbotage (aspirating and injecting technique to produce CSF turbulence) Age Gender Techniques Sitting, midline approach Sitting position is preferable in obese patients and other patients where the midline is difficult to determine. The upper end of the intergluteal sulcus can be used to determine the patient s midline. L4-5 interspace is usually at about 10 cm (4 inches) from the top of this sulcus (Franco). Using a hyperbaric solution in the sitting position and leaving the patient in that position for at least 5 minutes produces a saddle block. However, up to 20 minutes is necessary to wait in the desired position to achieve an appreciable lateralized or saddle distribution blockade. Lateral position It is the position of choice in many institutions. The patient lies on his/her side. It is more comfortable for the patient and decreases the risk for accidental fall and vasovagal problems. The technique otherwise is similar to sitting position Paramedian approach In some patients, especially elderly with calcified ligaments it is difficult to advance the thin spinal needle through the midline. The lateral approach is a good alternative in those cases. The spinous process is identified and the point of entrance is marked about 2 cm paramedian. The needle is directed slightly medial and cephalad. 35

36 Taylor Approach Usually the L5-S1 interspace is the larger. A spinal technique through it is known as Taylor approach. The entrance point is 1 cm medial and 1 cm caudal to the posterior superior iliac spine directing the needle cephalad and toward the midline. Anesthesia duration The local anesthetic used and the rate at which it is removed from the subarachnoid space determines duration. Elimination is entirely by vascular absorption and does not involve metabolism of LA within the subarachnoid space. Absorption occurs in the subarachnoid space itself and in the epidural space (local anesthetics cross the dura both ways). Side effects and Complications 1. Hypotension It is the most frequent side effect. It is mainly the result of venous pooling with decreased cardiac output due to sympathetic blockade. There is also a small component of arteriolar dilation. However systemic blood pressure does not decrease proportionally because of compensatory vasoconstriction especially in the upper extremities with intact sympathetic innervation. Even with total sympathetic blockade with spinal anesthesia the decrease in systemic vascular resistance is < 15%. This is because arterioles retain intrinsic tone and do not dilate maximally. The extent of decrease in BP is dependent on the extent of sympathetic blockade, intravascular volume, and cardiovascular status. Preloading the patient with ml while frequently used is supported by clinical studies. A mild vasopressor like ephedrine in 5-10 mg increments and fluid are all that is usually necessary to treat hypotension. Ephedrine is the drug of choice because it produces vasoconstriction and increased cardiac output. Phenylephrine is a good second choice especially if tachycardia is present. It causes vasoconstriction but could decrease the cardiac output. Trendelenburg position can alleviate the venous pooling but could produce an even higher spinal level. Flexion of the operating table with legs and back up is a good compromise. 2. Bradycardia When the sympathetic block reaches T2 level the cardioacelerator fibers are blocked and the vagus action is unopposed. The extent to which hear rate decreases in response to total sympathetic block during spinal usually is moderate (10-15%). However severe bradycardia and asystole have been reported in normal patients during otherwise uneventful spinal anesthesia. It can occur even in the absence of hypotension and can occur after minutes of spinal. The Bezold-Jarisch reflex has been implicated. This reflex would be triggered by 36

37 decreased venous return to the heart producing a paradoxical hypervagal response. Early recognition and treatment is essential. Ephedrine, atropine and in some cases epinephrine are indicated along with fluid replacement. 3. Total spinal Spinal anesthetic that involves the cervical region. It is manifested by respiratory arrest, bradycardia, hypotension and unconsciousness. The respiratory arrest most likely is a manifestation of ischemia of the medullary respiratory center secondary to intense hypotension and drop in cardiac output (complete sympathetic blockade) severe enough to compromise cerebral circulation. Block of phrenic nerve is not a likely cause. Management involves ABC with control of the airway, use of vasopressors, atropine and fluid replacement as needed. Miscellaneous physiologic effects 1. Respiratory Arterial gases are unaffected in patient breathing room air. Tidal volume, maximum inspiratory volumes and negative intrapleural pressure during inspiration are unaffected, despite intercostals muscle paralysis with high thoracic levels. This is because diaphragmatic activity remains intact. Expiratory volumes and total vital capacity are significantly diminished in high thoracic spinal, as are maximum intrapleural pressures during forced exhalation, and coughing. This is mainly due to paralysis of abdominal muscles. 2. Hepatic Hepatic blood flow decreases to the extent of hypotension to a degree similar than after general anesthesia. Spinal anesthesia has not proven to be an advantage or disadvantage in patients with liver disease. For intraabdominal surgery the decrease in hepatic perfusion is mainly due to surgical manipulation. 3. Renal Renal blood flow as cerebral blood flow is autoregulated through a wide range of arterial pressure. In the absence of renal vasoconstriction renal blood flow does not decrease until mean arterial pressure decreases below 50 mm Hg. Thus, in the absence of severe hypotension, renal blood flow and urinary output remain unaffected during spinal anesthesia. Loss of autonomic bladder control results in urinary retention. This is more frequent in males. 4. Endocrine and metabolic Spinal anesthesia, but not general anesthesia, blocks the hormonal and metabolic response associated with surgery. This response involves increases in ACTH, cortisol, epinephrine, norepinephrine and vasopressin as well as activation of the rennin-angiotensin-aldosterone system. However this effect seems to wear off along with the spinal anesthesia, producing metabolic and hormonal responses similar than after general anesthesia for the same operation. 37

38 5. Gastrointestinal The small intestine contracts during spinal and sphincters relax due to unopposed vagus nerve activity. The combination of contracted gut and complete relaxation of abdominal muscle provide good surgical conditions. Other effects and complications 1. Nausea Frequent side effect due to imbalance of sympathetic and parasympathetic visceral tone. Hypotension, bradycardia or hypoxia must be rule out. Antiemetics like ondansetron or droperidol are usually effective. 2. Post dural puncture headache (PDPH) PDPH is due to CSF leak through the dural puncture site. The subsequent loss of CSF pressure produces stretching of the meningeal coverings of intracranial nerves whenever the upright position is assumed. This plus the fact that the pain is relieved when the patient lies down is many times the only diagnostic tool. It is more frequent in females, in younger patients and during pregnancy. The size and type of needle are proven factors. Pencil point needles significantly reduce the risk. Spinal needles are either cut-bevel (Quincke-type) or pencil-point (Whitacretype). It has been usually accepted that the collagen fibers of the duramater are oriented longitudinally and that the bevel of a cutting needle should be oriented vertically to reduce trauma to the dural fibers. This concept has been challenged by Reina and collaborators (6). They found that dural fibers are arranged in laminas with fibers in different directions and not necessarily longitudinal. They also showed that pencil point needles produce a more traumatic lesion in the dura than cutting-point needles. They hypothesized that a more traumatic lesion will produce inflammation and that the subsequent edema would limit the leakage of CSF. This observation agrees with the surprisingly low incidence of PDPH after 18-gauge epidural needle is used for continuous spinal with a 20-gauge epidural catheter. The catheter might act as foreign object producing an inflammatory reaction. This low incidence can also at least in part reflect the fact that continuous spinal are more frequently performed in older patients. Older age has a decreased risk of PDPH. In summary: 1. Pencil point needles less than or equal to 22 gauge and cut-bevel needles less than or equal to 27 gauge produce an incidence of PDPH of approximately 1%. 2. Continuous spinal with 20 gauge catheters is not likely to produce PDPH in an older patient population. 3. Obstetric patients undergoing spinal anesthesia with small pencil point needles show a 3-4% rate of headache. Conservative treatment involves bed rest, IV or oral fluids Acetaminophen and NSAIDs are also used. Hydration and caffeine stimulates production of CSF. 38

39 4. Epidural blood patch with ml of autologous blood injected at the same level or one space below is very effective treatment. The effect can be immediate or be delayed by a few hours. A single blood patch is about 90% effective. 3. Transient neurological symptoms (TNS) Usually appears hrs after surgery and consist of mild to moderate pain or sensory abnormalities in the lower back, buttocks or lower extremities. It resolves between 6 hrs and 4 days. No patient with TNS has ever been reported to develop neurological deficits or motor weakness. If present other more serious diagnosis must be ruled out: epidural hematoma, nerve root damage. The first report appeared in the literature in 1993 when Schneider et al published a series of 4 patients with buttocks pain after spinal. Prospective, randomized studies have shown: 1. A higher (but variable) incidence after lidocaine spinal. Decreasing the concentration of lidocaine to 0.5% does not appear to change this incidence. 2. Its incidence seems related to other factors like: lithotomy (30-36%), knee arthroscopy (18-22%), whereas the risk after supine position appears to be relatively low (5 to 8%). The cause for TNS is not well understood and could represent a mild and reversible form of neuropathy. Many possible causes have been postulated: local anesthetic toxicity, needle trauma, neural ischemia secondary to sciatic nerve stretching, patient positioning, small gauge, pencil-point needles promoting local anesthetic pooling, muscle spasm, early mobilization, etc. Because of the low incidence of TNS after bupivacaine spinal, we could be reasonably sure than TNS is not the result of the subarachnoid block per se, the needle or the position for it. Even though neurotoxicity is frequently mentioned as possible cause for TNS, a case can be made against it. Cauda equina syndrome (CES) is known to result from local anesthetic toxicity; however the factors that increase CES, like higher doses and concentration of local anesthetics and the addition of vasoconstrictors, which increase CES, do not have an effect on TNS. We know that TNS is mostly associated with lidocaine spinal, lithotomy position, knee arthroscopy and ambulatory surgical status (obesity could be a contributing factor) and very rare after bupivacaine spinal. We also know that decreasing the concentration of lidocaine from 5% to 0.5% does not decrease the incidence of TNS and that hyperosmolarity, hyperbaricity and addition of glucose ARE NOT contributing factors. First line of treatment is reassurance, NSAIDs, comfortable positioning and heating pad. A second line of treatment can include narcotics and muscle relaxants like cyclobenzaprine. Trigger point injections have been used with reported success. Eliminating lidocaine from subarachnoid block probably is not warranted. However do not use it for ambulatory surgery in lithotomy position or knee 39

40 arthroscopy (high risk). On the other hand the incidence of TNS after inguinal hernia with lidocaine spinal is only 8%, C-section is 0-8% and tubal ligation is 3%, similar to non-pregnant patients undergoing surgery in the supine position. Bupivacaine even in small doses increases discharge time. Perhaps the combination of small doses of bupivacaine plus narcotics is the best possible approach. 4. Cauda equina syndrome It is a rare but devastating complication resulting in perineal anesthesia and possible loss of bowel and bladder control. Most of the reported cases have been associated with the use of continuous spinal with microcatheters (30-gauge and smaller) along with use of 5% hyperbaric lidocaine. Low flow rates promoting pooling of concentrated drug around the sacral roots has been postulated as the reason for this condition. In 1992 the FDA issued a safety alert that resulted in the withdrawal of these catheters from the US market. The incidence of CES increases with increased concentration of local anesthetics as well as the addition of vasoconstrictors. There have been reports of cauda equina syndrome after epidural anesthesia. 5. Back pain As many as 40% of patients may complain of this annoying side effect. It is postulated to be the result of stretching of the ligaments following the relaxation of back muscles. This is similar to what is seen in up to 25-30% of patients receiving general anesthesia in the supine position. It can also be the result of localized inflammatory response with muscle spasm. Rest, local heat and NSAIDs are the treatment of choice. 6. Hearing loss Transient minor hearing loss has been described after spinal anesthesia. The risk seems larger with larger-gauge needles and it might be the result of temporary decrease in CSF pressure with traction of intracranial nerves. The problem is mild but well documented with audiometry. It resolves on its own. 7. Infection Abscess or meningitis is rare. The development of meningitis after lumbar puncture in bacteremic patients is a concern. Animal models suggest that perioperative use of antibiotics eliminates this risk. Lumbar puncture in patients infected with HIV is controversial. Neuraxial techniques including blood patch have been perform on these patients without apparent problems. The risk has to be evaluated for individual patients. Spinal anesthesia in the outpatient setting A few years ago spinal anesthesia was favored for the outpatient setting. However readily available poorly-soluble general anesthetics and LMA have made the choice more difficult. Home readiness involves short duration of action and in many institutions 40

41 ability to void. Duration is a function of the agent and dose used. The spread of the agent dictates the duration at a given dermatome. It is likely that the more segments blocked by a given dose (more spread) the shorter the duration at any given segment. Hyperbaric solutions and isobaric solutions injected rapidly with the bevel turned caudad concentrates around the sacral roots and can delay sensory motor recovery and the ability to void. On a milligram basis, isobaric preparations injected rapidly with the bevel facing cephalad are more likely to improve home readiness and voiding. Intrathecal adjuncts 1. Epinephrine It prolongs duration but also prolongs the recovery time and voiding time. Thus it should not be used in the ambulatory setting. 2. Fentanyl The lipophilic synthetic opioids appear to improve the quality of the block without prolonging recovery (as opposed to epinephrine). Ben-David et al showed that 5 mg of hyperbaric bupivacaine was inadequate in 27% of cases of spinal for knee arthroscopy. Adding 10 ucg of fentanyl reduced the failure rate to zero. Fentanyl produces pruritus in about 50% of the patients. Serotonin inhibitors (like ondansetron) are being used to treat this side effect too. Respiratory effects are unlikely with < 25 ucg. 3. Morphine The use of hydrophilic intrathecal narcotics is accompanied by a longer lasting analgesia but also by a higher rate of complications. Among them are: delay respiratory depression (4-6 hrs after the injected dose), increased nausea and vomiting, pruritus and delayed voiding. 4. Clonidine and neostigmine They potentiate spinal local anesthetics and produce postoperative analgesia, but they produce unacceptably high rates of hypotension and sedation (clonidine) and protracted vomiting (neostigmine). 41

42 EPIDURAL ANESTHESIA It is technically more difficult to perform than spinal and because larger doses of local anesthetics are used it has the potential for systemic toxicity. On the other hand it offers a greater degree of flexibility in the extent and duration of anesthesia. Anatomy The spinal epidural space extends from the foramen magnum to the end of the dural sac at the level of S2. It is bounded anteriorly by the vertebral bodies and posteriorly by the laminae and ligamentum flavum. The epidural space outlines the spinal canal immediately superficial to the dura. In the cervical region the epidural space is smaller and wider in the lumbar area. A volume of local anesthetic about 10 times larger is required to produce lumbar epidural anesthesia than for equivalent subarachnoid blockade. Smaller volumes are sufficient for the thoracic space. The epidural space is filled with connective tissue, fat and veins, which can become enlarged during pregnancy. The spinal nerves travel through this space surrounded by a sheath of dura. Characteristic of an epidural blockade Epidural anesthesia produces a band of segmental anesthesia spreading cephalad and caudad from the site of injection. Epidural anesthesia has a slower onset and usually it is not as dense as spinal. This characteristic can be used as an advantage to obtain a more pronounced differential blockade. Dilute concentrations can spare the motor fibers while still able to produce sensory analgesia. This is commonly employed in labor epidural analgesia. Factors affecting the spread of local anesthetics in the epidural space In general 1-2 ml of local anesthetic is needed per every segment to be blocked. Thus, to achieve a T4 level from an L4-5 injection ml of LA is needed. 1. Dose and volume: The total dose and the volume affect the height of the block. The effect of volume is linear but it plateaus at about 20 ml, after which there is a greater loss through intervertebral foramina, especially in younger patients. 2. Age: As opposed to spinal, age is a major factor in the spread of epidural anesthesia with smaller volumes producing a higher spread in older patients. This may be due to the narrowing of the intervertebral foramina with age. 3. The site of injection influences the spread. Volumes as small as 6-8 ml of solution injected at the thoracic level can produce anesthesia due to smaller volume of the epidural space. 4. Body weight: heavier patients have smaller volume requirements. 5. Height: Plays a small role with taller patients requiring higher volumes. 6. Gravity: is not a very important factor, as sitting position does not appear to enhance sacral spread. Techniques Lumbar epidural The most common site for epidural anesthesia. The midline or paramedian approach can be used. A block below the termination of the spinal cord at L1 could be 42

43 safer. An accidental dural puncture ( wet tap ) could damage the spinal cord at higher levels. Thoracic epidural Technically more challenging. It has the risk of spinal cord injury. It is rarely used as the primary anesthetic. Many people prefer the paramedian approach because of the extreme obliquity of the thoracic spinous processes. Epidural needles The Tuohy needle is the most commonly used. A typical needle is gauge, 3.5 inches long, has a blunt bevel with a gentle curve at the tip of The blunt tip helps pushing the dura away tenting it after the ligamentum flavum has been pierced. Epidural catheters They provide the means for continuous infusion. Usually they are gauge in size. The bevel is directed in the desired location and the catheter is advanced 2-6 cm. The shorter the distance the greater the chance for accidental dislodgement. The further the distance the greater the chance of unilateral epidural and other complications (bloody tap, catheter knotting). Four to five cm is a good compromise. Test dose It is an important first step because of the relatively large doses injected into the epidural space. The classic test dose has 3 ml of 1.5% lidocaine (45 mg) with 1:200,000 of epinephrine (total of 15 ucg). The 45 mg of lidocaine if injected intrathecally should produce a spinal anesthesia. The 15 ucg of fentanyl should produce a 20% or more increase in the heart rate within 30 seconds or 30 beats between sec (Barash s, 5 th edition, 2006). In patients that are beta blocked the heart rate increase may not happen. In these patients an increased in systolic pressure of 20 mm Hg may be more reliable (Barash s 5 th edition, 2006). There is some controversy as to the possible systemic effects of epinephrine. In obstetrics some suggest using only 30 mg of lidocaine or 5 mg of bupivacaine as test dose. Activating an epidural Incremental dosing After a negative test dose most of practitioners will inject incremental doses of 5 ml at a time. This technique helps decrease the risk of systemic toxicity in case of catheter migration (intravascular or intrathecal). Termination of action It is related to type of drug and degree of spread. It is commonly described as the time it takes to a two-segment regression of sensory blockade. The approximate time for two-segment regression (sensory) for chloroprocaine is minutes, for lidocaine is minutes and for bupivacaine is minutes. 43

44 References 1. Snell s Clinical Anatomy for Medical Students, Barash s Clinical Anesthesia, 5 th edition, Mulroy s Regional Anesthesia, 3 rd edition Wong G, Brown D. Transient paraplegia following alcohol celiac plexus block. Reg Anesth 1995; 20: Hogan QH. Magnetic resonance imaging of cerebrospinal fluid volume and the influence of body habitus and abdominal pressure. Anesthesiology 1996;84; Cousin s Neural Blockade, 3 rd ed, Stoelting s Pharmacology and Physiology in Anesthetic Practice, 3 rd ed, Reina MA et al. An in vitro study of dural lesions produced by 25-gauge Quincke and Whitacre needles evaluated by scanning electron microscope. Reg Anesth Pain Med 2000:25; Swisher JL. Spinal Anesthesia: Past and Present. In Problems in Anesthesia, 2000:12; Ben-David et al. Intrathecal fentanyl with small-dose dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth Analg 1997: 85; Morgan s Clinical Anesthesiology, 4 th edition, Pollock JE. Transient neurological symptoms: etiology, risk factors, and management. Reg Anesth Pain Med 2002:27;

45 CHAPTER 4 REGIONAL ANESTHESIA AND ANTICOAGULATION Introduction 46 Guidelines summary consensus statement..47 New anticoagulants 51 References

46 Regional Anesthesia in the anticoagulated patient The American Society of Regional Anesthesia (ASRA) developed the 2 nd consensus statement on this topic in April 2002, published in May The statement focuses on anticoagulation and neuraxial blocks (spinal and epidural). The risk following plexus and peripheral techniques remains undefined. Epidural hematoma is defined as bleeding occurring around the spinal cord, which is a rare and potentially catastrophic complication of spinal or epidural anesthesia (it can happen spontaneously). Its incidence has dramatically increased in the United States since the introduction of low molecular weight heparin (LMWH). The following is a summary of the 2002 ASRA guidelines adapted from Neal JM: Neural blockade and anticoagulation. In: Regional Anesthesia, The requisites in anesthesiology. Rathmel J, Neal J, Viscomi C eds. Elsevier Mosby, Philadelphia, 2004 Anticoagulant ASRA guideline Catheter removal Evidence strength LMWH Single preop dose: Delay block h. Postop single daily dosing: Delay block 6-8 h. Postop twice daily dosing: Delay block 24 h Single daily dosing: Remove h after last dose; Wait 2 h before next dose Twice daily dosing: Remove 2 h before Pharmacokinetic data Large series of case reports Standard heparin Warfarin Aspirin/NSAIDs/COX-2 inhibitors Other antiplatelet agents Thrombolytics/ Fibrinolytics Fondaparinux (Arixtra) SQ 5,000 U/first dose: Delay heparin for 1-2 h after block. IV/first dose: Delay 1 h after block. IV/continuous: discontinue 2-4 h. Check aptt prior to block. New dose: check INR if 1 st dose given >24 h before or if 2 nd dose given. Chronic use: discontinue for 4-5 days. Check INR No issues if patient is not taking other anticoagulants Discontinue for: Ticlopidine (Ticlid): 14 days Clopidogrel (Plavix): 7 days Eptifibatide/tirofiban: 8 hrs Abciximab: 48 hrs Avoid a block within 10 days of drug administration. Avoid giving the drugs for 10 days after the block. If block was received around the time drug given, check neurological status 2 h Do not combine with neuraxial anesthesia first dose. Discontinue heparin for 2-4 h Check aptt prior to removal. If used for > 36 h, remove with INR <1.5 No issues No recommendation No recommendation No recommendation Pharmacokinetic data Prospective and retrospective case surveys and case reports Case series and case reports Retrospective case surveys Pharmacokinetic data Surgical recommendation No data Herbal supplements No specific concerns No issues No data 46

47 I encourage you to read the 2002 consensus statement as published in Regional Anesthesia and Pain Medicine in May-June Some highlights: 1. Fibrinolytic and thrombolytic therapy: plasmin originates from plasminogen and dissolves intravascular clots. Exogenous plasminogen activators, such as streptokinase and urokinase dissolve thrombus and affect circulating plasminogen. Endogenous t-pa formulations (alteplase and tenecteplase) are more fibrin-selective and have less effect on plasminogen. While the plasma halflife of thrombolytic drugs is only hours, it can take days for the thrombolytic effect to resolve; fibrinogen and plasminogen are maximally depressed at 5 hours after this therapy and remain significantly depressed at 27 hours. Contraindications to thrombolytic therapy include surgery or puncture of noncompressible vessels within 10 days. Recommendation: Patients on fibrinolytic and thrombolytic drugs should not receive spinal or epidural punctures. Data are not available to recommend a precise number of days. Ten days has been the usual recommendation. 2. Unfractionated heparin: the major anticoagulant effect of heparin is due to binding with antithrombin (AT). This effect leads to inactivation of thrombin (factor IIa), factor Xa, and factor IXa. IV injection results in immediate anticoagulant activity, whereas SC injection results in a 1 to 2 hour delay. The anticoagulant effect of heparin is typically monitored with aptt. Administration of small dose (5,000 U) SC heparin for prophylaxis of DVT generally does not prolong the aptt, and is typically not monitored. It can result in unpredictable 10-fold variability and therapeutic blood concentrations in some patients within 2 hours after administration. Intraoperative systemic heparinization: usually IV injection of 5 to 10,000 U. Recommendation: Performance of neuraxial procedure at least 1 hour prior to administration of heparin. Bloody or difficult placement may increase risk but there are no data to support mandatory cancellation of a case. Communication with the surgeon plus risk-benefit decision about proceeding is warranted. Heparinization into the postoperative may be continued and the risk of bleeding may be increased and so is the risk of spinal hematomas in the presence of a catheter (increased risk at removal). Indwelling neuraxial catheters should be removed 2 to 4 hours after the last heparin dose. Evaluation of the patient s coagulation status should be assessed before manipulation. Re heparinization should occur not before 1 hour after catheter removal Avoid neuraxial block in patients with other coagulopathies. Monitor the patient postoperatively for at least 12 hours 47

48 3. Complete anticoagulation during cardiopulmonary bypass: To date there are no cases of spinal hematomas associated with cardiopulmonary bypass. A review has recommended the following precautions: Avoid neuraxial blocks in patients with known coagulopathy of any cause Delay surgery for 24 hours in the event of a traumatic tap. Perform procedure at least 1 hour prior to systemic heparinization. Tightly control heparin doses and reversal doses to shortest duration compatible with desired effect Remove epidural catheter when normal coagulation is restored Closely monitor patients postoperatively for signs and symptoms of spinal hematomas. 4. Low-Dose SC heparin: commonly used for DVT prophylaxis in general and urologic surgery. A dose of 5,000 U of heparin every 12 hours has been used effectively. There is often no detectable change in aptt. Small percentage of patients (2-4%) may become therapeutically anticoagulated during SC heparin therapy. There is extensive experience in the US and Europe without complications. There are only 4 case reports of neuraxial hematomas in concomitance to the use of SC heparin. Recommendation: Performance of neuraxial block before the injection of SC heparin may be preferable. But there does not appear to be an increased risk in the presence of SC heparin. The risk may be increased in debilitated patients after prolonged therapy. 5. Low molecular weight heparin (LMWH): The biochemical and pharmacological properties of LMWH differ from those of unfractionated heparin. Most relevant are: no measured effect on anti-xa level, prolonged half-life and irreversibility with protamine. Since the introduction of LMWH in the United States in 1993 over 40 spinal hematomas were reported in association with its use over a 5-year period. This is in contrast with the European experience of only 13 spinal hematomas reported over a decade of extensive use. It should be noted that European dosing of LMWH is once daily, with the first dose administered 10 to 12 hours preoperatively. Recommendation: On patients receiving preoperative LMWH needle placement should occur at least 12 hr after last dose or 24 hr with higher doses Avoid neuraxial blocks in those patients receiving a dose of LMWH 2 hr preoperatively because needle placement would occur at peak anticoagulant activity. First dose of postoperative LMWH should be administered no earlier than 24 hr after the neuraxial procedure. Catheters should be removed prior to initiation of LMWH and first dose administered 2 hr after catheter removal 48

49 If patient has been receiving a single daily dose catheter can be safely maintained. However it should be removed a minimum of 12 hr after the last dose and the subsequent dose a minimum of 2 hr after catheter removal. 6. Oral anticoagulants (warfarin): They interfere with the synthesis of vitamin K-dependent clotting factors: II (thrombin), VII, IX, X. The effects of warfarin are not apparent until a significant amount of biologically inactive factors are accumulated and is dependent on factor half-life: Factor VII: 6 to 8 hr Factor IX: 24 hr Factor X: 25 to 60 hr Factor 2: 50 to 80 hr Factor activity level of 40% for each factor is adequate for normal hemostasis. The PT and INR are most sensitive to the activities of factors VII and X and are relatively insensitive to factor II. Because factor VII has a short half-life prolongation of PT and INR may occur in 24 to 36 hr. Prolongation of the INR (INR > 1.2) occurs when factor VII is down to 55% of baseline, while an INR of 1.5 is associated with factor VII activity of 40%. Thus an INR < 1.5 should be associated with normal hemostasis. Upon discontinuation of warfarin factor VII activity will rapidly increase and the INR will decrease. However factor II and X recover much more slowly, thus hemostasis may not be adequate even though the INR is 1.4 or less. Adequate levels of all vitamin K-dependent factors are typically present when the INR <1.2. In emergency situations the effect of warfarin can be reversed by vitamin K injection and/or transfusion of fresh frozen plasma. Recommendation: Do not perform neuraxial blocks on patients who have been on chronic warfarin therapy. Caution should be exercised when patients have had their warfarin discontinued prior to surgery. Ideally 4 or 5 days should elapse and PT and INR should be measured prior to any neuraxial block. Remember that early after warfarin discontinuation the PT/INR reflect predominantly factor VII levels while the rest of factors activity is still inadequate. Wait until PT/INR are normal. Concurrent use of medication that affect other components of the clotting mechanism may increase the risk of bleeding and do so without affecting PT/INR (aspirin and other NSAIDs, ticlopidine and clopidogrel). Patients receiving one initial dose more than 24 hr prior to block should have PT/INR checked before proceeding. As thromboprophylaxis with warfarin is initiated with a catheter in place during low dose warfarin therapy, PT/INR should be checked daily and before catheter removal. The INR prior to removal should be less than 1.5. Continue neurological exams at least 24 hr after removal. 49

50 7. Antiplatelets medications: include: NSAIDs (aspirin, ibuprofen, others) Thienopyridine derivatives like ticlopidine (Ticlid) and clopidogrel (Plavix) Platelet GP IIb/IIIa receptor antagonists (abciximab, eptifibatide and tirofiban). - NSAIDs inhibit platelet cyclooxygenase (COX) and prevent the synthesis of thromboxane A2. COX exists in 2 forms; COX-1 regulates constitutive mechanisms, while COX-2 mediates pain and inflammation (no effect on platelets). Platelet function is affected for the life of the platelet following aspirin; other nonsteroidals (naproxen, ibuprofen) have a short-term effect (3 days). - COX-2 inhibitors like celecoxib (Celebrex) and rofecoxib (Vioxx) are antiinflammatory agents that affect COX-2 an enzyme not present in platelets, and thus do not cause platelet dysfunction. - The thienopyridine derivatives have antiplatelet effect from inhibition of ADP-induced platelet aggregation. These agents are used in the prevention of cerebrovascular thromboembolic events. Labeling recommends, if a patient is to undergo elective surgery, and an antiplatelet effect is not desired, clopidogrel should be discontinued 7 days and ticlopidine days prior to surgery. - Platelet GP IIb/IIIa receptor antagonists inhibit platelet aggregation by interfering with platelet-fibrinogen and platelet-von Willebrand factor binding. Time to normal platelet aggregation ranges from 8 hr (eptifibatide, tirofiban) to 24 to 48 hr (abciximab). Labeling precautions recommend that puncture of noncompressible sites and epidural be avoided. Recommendation: Difficult to generalize because these drugs have different effects There is no accepted test to guide antiplatelet therapy. NSAIDs: their use alone does not seem to create a level of risk that will interfere with the performance of neuroaxial blocks. At this time there is no specific concern as to the timing of single-shot or catheter techniques or the timing of catheter removal in conjunction with NSAIDs. Thyenopyridine derivatives: risk unknown. Follow labeling precautions: clopidogrel (Plavix) 7days and ticlopidine (Ticlid) 14 days. GP IIb/IIIa antagonists: risk unknown. Follow label precautions: 48 hr for abciximab and 4-8 hr for eptifibatide and tirofiban The concurrent use of other medications affecting clotting may increase the risk of bleeding complications. 8. Effect of herbal therapies on coagulation: The use of herbal medications is widespread in surgical patients. Garlic: inhibits platelet aggregation in a dose dependent fashion. Its effect appears to be irreversible and may potentiate the effect of other platelet inhibitors. There is one case of epidural hematoma in an octogenarian that was attributed to heavy garlic use. Ginkgo: Appears to inhibit platelet-activating factor (PAF). Four cases of spontaneous intracranial bleeding have been associated with ginkgo use. 50

51 Ginseng: inhibit platelet aggregation in vitro and prolongs Thrombin time and activated partial thromboplastin time in rats. These findings need to be confirmed in humans. On the other hand it was associated to a significant decrease in warfarin anticoagulation in 1 reported case. Recommendation: Herbal drugs by themselves appear to represent no added significant risk for spinal hematomas in neuraxial blocks. Mandatory discontinuation or cancellation of surgery is not supported by available data. Concurrent use of other medications affecting clotting may increase the risk of bleeding. No specific concern about timing of neuraxial catheter removal. New Anticoagulants (Direct Thrombin Inhibitors and Fondaparinux), from ASRA website (January 2006): New antithrombotic drugs which target various steps in the hemostatic system, are continually under development. The most extensively studied are antagonists of specific platelet receptors and direct thrombin inhibitors. Many of these agents have prolonged half-lives and are difficult to reverse without administration of blood components. Thrombin inhibitors Recombinant hirudin derivatives, including desirudin, lepirudin, and bivalirudin inhibit both free and clot-bound thrombin. Argatroban, an L-arginine derivative, has a similar mechanism of action. Although there are no case reports of spinal hematoma related to neuraxial anesthesia among patients who have received a thrombin inhibitor, spontaneous intracranial bleeding has been reported. Due to the lack of information available, no statement regarding risk assessment and patient management can be made. Identification of interventional cardiac and surgical risk factors associated with bleeding following invasive procedures may be helpful. Fondaparinux Fondaparinux produces its antithrombotic effect through factor Xa inhibition. The FDA released fondaparinux with a black box warning similar to that of the LMWHs and heparinoids. The actual risk of spinal hematoma with fondaparinux is unknown. Consensus statements are based on the sustained and irreversible antithrombotic effect, early postoperative dosing, and the spinal hematoma reported during initial clinical trials. Close monitoring of the surgical literature for risk factors associated with surgical bleeding may be helpful in risk assessment and patient management. Until further clinical experience is available, performance of neuraxial techniques should occur under conditions utilized in clinical trials (single needle pass, atraumatic needle placement, avoidance of indwelling neuraxial catheters). If this is not feasible, an alternate method of prophylaxis should be considered. 51

52 References 1. Anesthesiology Clinics of North America 2000: 18(2); Neal JM: Neural blockade and anticoagulation. In: Regional Anesthesia, The requisites in anesthesiology. Rathmel J, Neal J, Viscomi C eds. Elsevier Mosby, Philadelphia, 2004, pages Consensus statement on Anticoagulation and Regional Anesthesia. Reg Anesth Pain Med 2003;28:172-97Anticoagulation and neuraxial regional anesthesia: perspectives. [Editorial] Regional Anesthesia and Pain Medicine 28(3);163-6, 2003 May-Jun. 4. Horlocker et al. Regional anesthesia in the anticoagulated patient: defining the risks (The second ASRA consensus conference on neuraxial anesthesia and anticoagulation. Regional Anesthesia and Pain Medicine 28(3);172-97, 2003 May-Jun. 52

53 CHAPTER 5 PERIPHERAL NERVE BLOCKS Bringing the needle close to its target Nerve stimulators.54 Insulated versus non-insulated needles 55 Ultrasound 55 Short versus long-bevel needles...56 Nerve injury References 59 53

54 Peripheral Nerve Blocks Injecting an adequate volume and concentration of local anesthetic in the proximity of the target nerve(s) leads to a successful peripheral nerve block. Intraneural injection (injection inside the nerve) is harmful to the nerve and can lead to permanent damage. Thus a balance must be achieved between proximity and safety. Bringing the needle close to the nerve(s) There are many ways to ascertain the correct placement of a needle with respect to the nerve. A good knowledge of the anatomy makes things easier and safer. The methods are: 1. Purely anatomical: the practitioner bases his/her technique solely on anatomical facts to bring the needle in proximity to the nerve. For example, the median nerve at the elbow is located just medial to the brachial artery. Thus finding the pulse at the elbow is an important landmark. Another example is the femoral artery in the groin and its constant relationship to the femoral nerve located lateral to it. Locating the femoral pulse helps to find the nerve. The trans-axillary technique of brachial plexus block is another good example. Knowing that the terminal branches of the brachial plexus surround the axillary artery in a very predictable pattern is used to block the plexus. This anatomical method practiced alone has limited success because it does not take into account anatomical variations, lacks depth perception and can not gauge proximity to the nerve with any degree of certainty, thus the needle might end too far from the nerve (failed block) or too close (intraneural). 2. Paresthesia: this technique is a combination of anatomical knowledge and patient collaboration. The needle is brought to the point of physical contact with the target nerve. The patient is instructed to acknowledge the electrical sensation elicited (paresthesia). The location of the paresthesia tells the practitioner the location of the needle. At this time the needle is withdrawn a few mm before the injection is started to prevent intraneural injection. For the longest time this was the preferred technique. Dr. Moore s dictum no paresthesia no anesthesia became the law of the land with respect to regional anesthesia. Starting in the 1970 s with the work of Dr Selander demonstrating nerve damage of different magnitude by the probing needle, the safety of a paresthesia technique has come into question. Up to date there is not enough clinical evidence to support the idea that paresthesias lead to nerve damage. However there seems to be enough circumstantial evidence to be cautious especially if repeated paresthesias are elicited. 3. Nerve stimulator: the idea of locating mixed nerves by electrical stimulation was developed in Germany in the 1910 s. However it was not until 1962 when Greenblatt and Denson introduced a portable nerve stimulator that was suitable for the clinical setting. 54

55 The nerve stimulator is connected to a needle, usually insulated, that delivers a current to its tip. The A alpha fibers (motor) are readily depolarized by the small currents used but not the sensory fibers. As the needle approaches a mixed nerve a painless muscle twitch is produced. The intensity of the response is inversely proportional to the needle tip-nerve distance (actually to the square root of it). Thus a visible response at lower currents ( 0.5 ma) suggests close proximity between the needle tip and the target nerve. There is a good amount of clinical evidence to suggest that a current of 0.5 ma or less, able to produce a visible response means enough proximity to produce a block. However evidence is lacking as to what exactly that distance is and as to whether the distance is different for different nerves. In general it is thought that 1 ma of current will produce depolarization of a motor nerve at a distance of about 1 cm (10 mm). Nowadays nerve stimulator techniques are widely practiced around the world. Because they do not necessarily rely on patient cooperation, they are sometimes used in unconscious or heavily sedated patients. We do not encourage this practice as it can lead to complications that a conscious patient could help prevent (e.g., intraneural injection). With modern nerve stimulators the practitioner can adjust the pulse intensity (magnitude of the current) in ma; the pulse frequency (amount of pulses per second) in Hz (1 or 2) and the pulse width (duration of the pulse) in milliseconds (ms). The pulse duration most suitable for stimulating motor fibers in a mixed nerve is 0.1 ms (100 µs). Insulated versus non-insulated needles: Insulated needles (Teflon-coated) are the needles most commonly used in conjunction with a nerve stimulator in the United States and Europe. The current applied to this needle concentrates on the tip of it making the localization of nerves more accurate. Several brands of these needles exist in the market and they come ready with a connection that only fits the negative electrode. Connecting the negative electrode to the exploring needle lowers the amount of current necessary to depolarize a nerve. Non-insulated needles transmit the current preferentially to the tip but also along the shaft of the needle making the localization of nerves less accurate. Insulated needles are more expensive than non-insulated needles. 4. Ultrasound: It is the latest development in regional anesthesia and it is the only method that provides real time assessment of the position of the needle with respect to the nerve as well as visualization of the surrounding structures. An added advantage is that the practitioner is able to see the distribution of the local anesthetic around the target nerve(s), thus predicting more accurately whether the block will be successful or supplementation will be necessary. Ultrasound is still expensive, and requires competency on interpretation of cross-section anatomy from images that could be grainy and confusing. Ultrasound could theoretically produce warming of tissues or gas formation. The technology has been progressing rapidly and it should be a matter of time before it becomes a method of choice. The human ear can hear sounds between 20 and 20,000 cycles per second (Hz). Ultrasounds waves travel at a higher frequency than the highest frequency 55

56 that the human ear can detect which is 20,000 Hz or 20 KHz. Ultrasound waves used in medicine usually are in the 1 to 20 MHz range (1 MHz= 1 million Hz). High frequency waves are shorter and good for superficial structures. Ultrasound waves travel easily through fluids and soft tissue but have problems traveling through bone and air. Ultrasound is better reflected at the transition between two different types of tissues like soft tissue-air, bone-air and soft tissue-bone. The ultrasound is delivered from a small probe that contains a transducer. The transducer converts electrical signals into ultrasound waves and then detects the reflected waves and converts them back into electrical signals, which are eventually the source of the image we see on the screen. So the transducer part of the time delivers ultrasound and part of the time listens for the returned waves. Some of the wave sounds pass through the tissues while others get reflected back into the transducer. The distance is a function of the time it takes for the wave to return. Tissues with high density like bones reflect most of the waves and produce a bright image. These tissues are known as hyperechoic. The hypoechoic structures are soft tissue structures with different degrees of echo. The more perpendicular the probe is to the structure (e.g., nerve) being searched, the better the image, because more bouncing sound waves can be detected by the transducer. This is also true when trying to visualize the needle. Changes as small as 10 degrees from the perpendicular can distort the quality or echogenicity of a nerve by reducing the amount of waves bouncing out of the nerve back into the transducer. The easiest way to identify a peripheral nerve is on a transverse scan, also called short axis view. The needle on the other hand can be advanced with the out-of-plane approach in which the needle crosses the ultrasound beam perpendicularly. The needle becomes practically invisible, as its cross section is one more of the thousands of dots that form the ultrasound image. With the in plane approach the needle is advanced parallel to the probe. Depending on its depth and angle of insertion the whole needle can be visualized. With either approach the needle is aimed to the nerve surroundings. Scanning superficial structures like the brachial plexus requires high frequency probes (10-15 MHz) that provide good resolution but limited penetration (3-4 cm). For deeper structures like the brachial plexus in the infraclavicular region or sciatic nerve in the buttocks lower frequencies (4-7 MHz) are needed. Deep scanning of intra abdominal organs requires frequencies of 3-5 MHz. Short versus long-bevel needles Standard needles have an angle of around 14 degrees and are known as sharp needles. It is frequently recommended to perform regional block with short-bevel needles with an angle of 30 to 45 degrees. This recommendation comes from studies by Selander et al who demonstrated more neural damage in isolated sciatic nerves when sharp needles were used. The damage with sharp needles was also more extensive when the orientation of the sharp bevel was perpendicular to the fibers. With short bevel the damage was less frequent as the fibers tend to be pushed away by the advancing needle. 56

57 This concept has been challenged. It could be more difficult to penetrate a nerve with a short-bevel needle, but it is likely that when it happens the resulting damage may be greater. Nerve injury (Adapted from Horlocker s chapter 11 in Complications in Regional Anesthesia edited by John L. Atlee): Nerve damage can occur after regional anesthesia, although severe or disabling neurologic injury rarely occurs. Kroll et al in 1990 reviewed the American Society of Anesthesiologist closed-claims database. He found that out of 1541 claims 227 (15%) were for anesthesia-related injury. Ulnar neuropathy was the most frequent nerve injury (33%) and was related to general anesthesia. Brachial plexus injury was claimed in 23% and lumbosacral in 16%. Regional anesthesia was more frequently involved in claims involving nerve damage (82/227 or 36.1%). When a claim different than nerve damage was made regional anesthesia was involved in 22.5% (296/1314). The mechanisms by which regional anesthesia results in nerve damage are: 1. Needle or catheter trauma 2. Local anesthetic toxicity 3. Neural ischemia 4. Infection Nerve damage can occur perioperatively for a reason other than regional anesthesia, like: 1. Surgical trauma 2. Use of retractors 3. Positioning 4. Tourniquet ischemia 5. Improperly placed dressings or casts 6. Preexisting neurologic condition Use of epinephrine Epinephrine containing local anesthetic solutions may theoretically produce nerve ischemia by vasoconstriction of the epineural and peri-neural blood vessels. Patients at increased risk would be those with previous impaired microcirculation (e.g., diabetics). There is no consensus as to how important this factor is in clinical practice. An adequate assessment of risks and benefits has to be made when using vasoconstrictors especially in high-risk populations (see discussion on local anesthetic chapter). Persistent Paresthesia, Clinical presentation (Adapted from Selander s chapter 7, in Complications of Regional Anesthesia, edited by Brendan T. Finucane): 57

58 The symptoms can appear within 24 h or may not become apparent until days or weeks after the offending procedure took place. The intensity and duration of symptoms vary with the severity of the injury, from short lasting intermittent tingling and numbness to persistent and painful paresthesias or dysesthesias lasting months or years. Pre-existing neurologic condition and regional anesthesia A pre existing neurologic condition per se is not a contraindication to regional anesthesia. However a careful preoperative assessment must be made, including a careful and descriptive neurologic evaluation and documentation. Patient should be made aware of potential risks as well as the potential for perioperative neurologic symptoms that could develop unrelated to the regional anesthesia technique. Certain unstable neurologic conditions like: multiple sclerosis, acute poliomyelitis, amiotrophic lateral sclerosis, Guillian Barre syndrome may develop new symptoms perioperatively totally unrelated to anesthesia. In these cases the risks and benefits must be carefully evaluated. There are other stable neurologic conditions like a preexisting peripheral neuropathy, inactive lumbosacral radiculopathy and neurologic sequelae of stroke that can be adequately managed with regional anesthesia. Persistent Paresthesia Prevention Several factors affect the outcome of regional anesthesia. In order to prevent neurologic injury especial attention must be paid to: 1. Patient selection 2. Surgeon selection 3. Meticulous technique 4. Avoidance of direct needle trauma and intraneural injection 5. Risk/benefit of vasoconstrictors 6. Appropriate local anesthetic concentration When a perioperative neuropathy develops a prompt evaluation is necessary and a multidisciplinary approach is recommended with participation of neurology, radiology, and surgery. 58

59 References 1. Mulroy s Regional Anesthesia, 3 rd edition Selander D, Dhuner KG, Lundborg G. Peripheral nerve injury due to injection needles used for regional anesthesia. Acta Anaesth Scan 1977; 21: Cousin s Neural Blockade, 3 rd ed, Stoelting s Pharmacology and Physiology in Anesthetic Practice, 3 rd ed, Finucane s Complications of Regional Anesthesia, Morgan s Clinical Anesthesiology, 4 th edition, Horlocker s chapter 11 in Complications in Regional Anesthesia edited by John L. Atlee 8. Textbook of Regional Anesthesia. Hadzic A ed. New York, McGraw Hill, ASA Refresher Courses in Anesthesiology. Chapter 14 59

60 CHAPTER 6 UPPER EXTREMITY NERVE BLOCKS Anatomy of the brachial plexus 61 Interscalene muscles.61 Distribution of brachial plexus branches..62 Interscalene block.64 Supraclavicular block 68 Infraclavicular block..74 Axillary block 77 References.80 60

61 UPPER EXTREMITY BLOCKS Anatomy of the brachial plexus Roots The brachial plexus is most commonly formed by five roots originating from the ventral divisions of C5 through T1. The roots of the plexus are located in the cervical paravertebral space between the anterior and middle scalene muscles. It is important to understand the plexus also in terms of its relative surface area at different levels of its trajectory. As shown in figure 6.1 each root of the plexus emerges from an intervertebral foramen. The C5 root appears between cervical vertebrae 4 and 5, while the T1 root emerges between thoracic vertebrae 1 and 2. Fig 6.1. Cadaver dissection of left supraclavicular area. The sternocleidomastoid and anterior scalene muscles have been removed. The subclavian artery and the vertebral artery appear painted in red. The suprascapular nerve is the branch seen coming off the upper trunk. The pleural dome is painted blue. (Own dissection). The distance from C5 to T1 roots is large and irreducible, and equal to the height of four vertebrae. This fact helps to explain why an interscalene block, which is usually performed at C5 or C6 level, would frequently miss dermatomes C8-T1 simply because they are too far from the site of injection. Another important reason in many patients is the pulsatile effect of the subclavian artery over the C8 and T1 roots preventing the local anesthetic from reaching them. When the five roots combine together to form three trunks not only there is a 40% reduction in the number of nerve structures (from 5 to 3) but also the trunks become physically contiguous. This is the point where the brachial plexus is reduced to its smallest surface area and helps to explain the rapid onset and high success rate of the supraclavicular approach. This special circumstance is only seen in the brachial plexus and has not parallel in the lower extremity. The surface area of the plexus increases again when the trunks originate one posterior and one anterior division each and further when the plexus ends giving off terminal branches in the axilla. The scalene muscles The anterior scalene muscle originates in the anterior tubercles of the transverse processes of C3 to C6 and inserts on the scalene tubercle of the upper surface of the first rib. The middle scalene muscle originates in the posterior tubercles of the transverse processes of C2 to C7 and inserts on a large area of the upper surface of the first rib behind the subclavian groove. 61

62 Trunks to terminal branches The five roots converge toward each other to form three trunks -upper, middle and lower-stacked one on top of the other as they traverse the triangular interscalene space formed between the anterior and middle scalene muscles. This space becomes wider in the anteroposterior plane as the muscles approach their insertion on the first rib. While the roots of the plexus are long, the trunks are almost as short (1-2 cm) as they are wide, soon giving rise to a total of six divisions (three anterior and three posterior) as they reach the clavicle. The area of the trunks corresponds to the point where the brachial plexus is confined to its smallest surface area, three nerve structures, closely related to one another, carrying the entire sensory, motor and sympathetic innervation of the upper extremity with the exception of a small area in the axilla and upper middle arm (intercostobrachial nerve, a branch of the second intercostal nerve). This special arrangement is mandated by the narrow passage between the clavicle and the first rib that the neurovascular bundle must negotiate before getting into the axilla. The brachial plexus enters the apex of the axilla next to the axillary artery, which is the continuation of the subclavian artery. At this point the divisions rearrange and mixed their fibers to form three cords, lateral, medial and posterior, named after their relative position to the axillary artery. The cords travel caudally in close proximity to the coracoid process, under the cover of the pectoralis minor muscle, which itself is covered by the pectoralis major muscle. At about the level of the lateral border of the pectoralis minor muscle the three cords give off their terminal branches. The posterior cord originates the axillary and radial nerves; the medial cord originates part of the median nerve, plus the ulnar, medial brachial and medial antebrachial cutaneous nerves. The lateral cord originates the rest of median nerve and musculocutaneous nerve. Very often the musculocutaneous nerve remains attached to the median nerve until reaching the proximal arm. Distribution of the branches of the brachial plexus Axillary nerve (C5-C6): gives an articular branch to the shoulder joint, motor innervation to the deltoid and teres minor muscles and sensory innervation to part of deltoid and scapular regions. Radial nerve (C5-C6-C7-C8-T1): supplies the skin of the posterior and lateral arm down to the elbow, the posterior forearm down to the wrist, lateral part of the dorsum of the hand and the dorsal surface of the first three and one-half fingers proximal to the nail beds. It also provides motor innervation to the triceps, anconeus, part of the brachialis, brachioradialis, extensor carpi radialis and all the extensor muscles of the posterior compartment of the forearm. Its injury produces a characteristic wrist drop. Median nerve (C5-C6-C7-C8-T1): gives off no cutaneous or motor branches in the axilla or the arm. In the forearm it provides motor innervation to the anterior compartment except the flexor carpi ulnaris and the medial half of the flexor digitorum profundus (ulnar nerve). In the hand provides motor innervation to the thenar eminence and the first two lumbricals. It provides the sensory innervation of the lateral half of the palm of the hand and dorsum of first three and one-half fingers including the nail beds. 62

63 Ulnar nerve (C8-T1): like the median nerve, the ulnar nerve does not give off branches in the axilla or the arm. Its motor component supplies the flexor carpi ulnaris and the medial half of the flexor digitorum profundus. In the hand it provides the motor supply to all the small muscles of the hand except the thenar eminence and first two lumbricals (median). Its sensory branches supply the medial third of the dorsum and palmar sides of the hand and dorsum of the 5 th finger and dorsum of the medial side of 4 th finger. Medial brachial cutaneous nerve (T1): it is solely a sensory nerve. It supplies the skin of the medial side of the arm. It is joined here by the intercostobrachial nerve, branch of the second intercostal. Medial antebrachial cutaneous nerve (T1): It is also a sensory nerve. It supplies the medial side of the anterior forearm. Musculocutaneous nerve (C5-C6-C7): gives motor innervation to the choracobrachialis, biceps and brachialis muscles. At the elbow it becomes purely sensory innervating the lateral anterior aspect of the forearm to the wrist. Pearls With the shoulder down the three trunks of the brachial plexus are located above the clavicle, thus the blocking needle during a supraclavicular block should never need to reach below the clavicle. For the most part the first intercostal space is located below the clavicle (with the exception of the most posterior paravertebral part), thus its penetration is unlikely during a properly performed supraclavicular block. The needle should never cross medial to the parasagital plane of the anterior scalene muscle because of risk of pneumothorax. The pulsatile effect of the subclavian artery exerted mainly against C8-T1 roots and the lower trunk explains why the C8-T1 dermatome can be spared during a supraclavicular block if the injection is not performed in the vicinity of the lower trunk (fingers twitch with nerve stimulator or behind subclavian artery with ultrasound). The SCM muscle inserts on the medial third of the clavicle, the trapezius muscle on the lateral third of it, leaving the middle third for the neurovascular bundle. These proportions are maintained regardless of patient s size. Bigger muscle bulk through exercise does not influence the size of the muscle insertion area. The brachial plexus crosses the clavicle at or near its midpoint. Because of the direction of the brachial plexus from medial to lateral as it descends, the higher in the supraclavicular area the more medial (closer to the SCM) the plexus is located. 63

64 INTERSCALENE BLOCK Indications Its main indication is anesthesia of the shoulder, lateral part of the clavicle and proximal part of the humerus. Point of contact of the needle with the brachial plexus The needle approaches the plexus at the level of the roots, high in the interscalene groove, approximately at the level of C5-C6 roots (most likely C5). Main characteristics This block is superficial and usually easy to perform. Characteristically it misses the C8-T1 dermatome, which includes ulnar nerve, medial antebrachial cutaneous nerve and medial brachial cutaneous nerve. Patient position and landmarks The patient is lightly sedated. Older, obese and recent trauma patients can be expected to be extremely sensitive to the depressant effects of benzodiazepines and/or narcotics. Titrate to effect. The patient lies supine or on a 30-degree upright position. The ipsilateral shoulder is down and the head is turned slightly to the opposite side. The posterior (lateral) border of the sternocleidomastoid (SCM) muscle is identified as well as the upper border of the cricoid cartilage, as shown in figure 6-2. Fig 6-2. Cricoid cartilage. The superior border of the cricoid cartilage at the level of the cricothyroid membrane is marked on the skin. (On a model with permission). A horizontal line is drawn from the cricothyroid membrane laterally to intersect the posterior border of the SCM. The index and middle fingers of the palpating hand are placed behind the SCM at this level pushing it slightly forward, as shown in figure 6-3. This maneuver brings the palpating fingers behind the SCM and on top (anterior) to the anterior scalene muscle. The fingers are then rolled back until they fall into the interscalene groove, which at this proximal point in the neck is a real structure and it is easy to identify. This is the point of needle insertion. 64

65 Fig 6-3. Finding the interscalene groove. The interscalene groove is found behind the SCM at the horizontal level of the cricoid cartilage. (On a model with permission). Nerve stimulator technique The nerve stimulator is set to deliver a current of ma, at a pulse frequency of 1 Hz and a pulse width of 0.1 ms (100 µs). A small skin wheal is raised with 1% lidocaine or 1% mepivacaine using a small gauge needle (ideally 27). A 2 (5 cm) or 1 (2.5 cm), 22-gauge, short bevel, insulated needle can be used. The needle is introduced between the two palpating fingers in a medial direction that also has a small (20 to 30-degree) posterior and caudal inclination, as shown in figure 6-4. Fig 6-4. Needle insertion. The needle is advanced medial, posterior and caudal. (On a model with permission). A needle directed just medial has a bigger chance to enter the intervertebral foramen and produce intravascular injection (vertebral artery) or penetrate the subarachnoid and epidural spaces. Any distal motor twitch as well as biceps, triceps or deltoid muscles are adequate. A twitch of the abdomen signals phrenic nerve stimulation and it is evidence that the needle is anterior to the anterior scalene. The needle should be withdrawn and redirected posteriorly. A motor twitch of the trapezius muscle indicates stimulation of the spinal accessory nerve and signals that the position of the needle is posterior to the brachial plexus and needs to be repositioned anteriorly. The injection of the local anesthesia is started slowly with frequent aspirations. There is some confusion as to whether a shoulder twitch is acceptable. Anatomical and clinical evidence support accepting any twitches other than trapezius (please see: Silverstein W et al. Interscalene block with a nerve stimulator: A deltoid motor response 65

66 is a satisfactory endpoint for successful block. Reg Anesth Pain Med 2000; 25: and accompanying editorial by William Urmey, same journal page ). Ultrasound technique The area is best visualized by placing the probe obliquely across the anterior and middle scalene muscles at the level of C5-C6. The SCM is identified as well as the great vessels (common carotid and internal jugular). The internal jugular vein is easily collapsible by the probe, which helps with its identification. Behind and somewhat lateral to the SCM the anterior and middle scalene muscles are usually easily visualized and the roots of the plexus appear in between them. The needle is advanced in plane with the probe from lateral to medial with a slight posterior and caudal deviation, similar to Winnie s approach. The needle is advanced under direct visualization into the proximity of C6 root and the spread of local anesthetic should show the interscalene space expanding. Local anesthetic and volume For single shot techniques in adults, 30 ml of 1.5% mepivacaine plain provides 2-3 h of anesthesia. The addition of 1:400,000 epinephrine prolongs the anesthesia to about 3-4 h. The residual analgesia post anesthesia is variable in duration although rarely persists for more than 2 h after block resolution. Ropivacaine 0.5% % can be used in the same volume to provide 5-7 h of anesthesia. The addition of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine accomplishes similar extended duration with shorter onset, although the onset is longer than for mepivacaine alone. Also ml of 0.2% ropivacaine can be used to provide postoperative analgesia for surgery performed under general anesthesia. Side effects and complications Systemic local anesthetic reaction can occur as with any block. More specific (and frequent) side effects related to interscalene block are: Horner s syndrome (ptosis, miosis and anhydrosis) due to stellate ganglion block and hoarseness due to recurrent laryngeal nerve involvement. Characteristically this block produces 100% of phrenic nerve block with diaphragmatic paralysis (Urmey W. et al. One hundred percent incidence of hemidiaphragmatic paresis associated with interscalene brachial plexus anesthesia as diagnosed by ultrasonography. Anesth Analg 1991; 72: ). This can produce dyspnea and reductions in respiratory volumes of up to 30%. Pneumothorax is possible but rare with this block. Clinical pearls Because of the position of the shoulder so close to the head of the patient, the anesthesiologist must carefully evaluate the patient and surgeon before deciding whether an interscalene block could be a good choice as the only anesthesia for the case. It must be remembered that most of these procedures are performed in positions other than supine (e.g., beach chair, prone, lateral) thus management of the airway 66

67 is a concern. A surgeon not familiar with shoulder surgery under regional anesthesia is a concern, as rough maneuvers could make the patient uncomfortable. Language barrier between patient and anesthesiologist is also a relative contraindication. This is a very superficial block. Care should be taken not to introduce the needle more than 2-3 cm beyond the projection of the midpoint of the SCM muscle. Although ultrasound provides a way of improving anesthesia at the level of C8-T1 dermatomes with interscalene block, I still prefer supraclavicular block for any anesthesia of the upper extremity beyond the shoulder. 67

68 SUPRACLAVICULAR BLOCK Indications This block is ideally suited for any surgery on the upper extremity that does not involve the shoulder. Point of contact of the needle with the brachial plexus The needle approaches the plexus at the level of the trunks and ideally the injection should take place in the vicinity of the lower trunk. Main characteristics This block is considered more difficult to learn and historically has been associated with a higher risk of pneumothorax. The literature cites rates between percent. However with good anatomy and meticulous technique we have been able to practically almost eliminate this risk. A supraclavicular block is usually associated with a short onset and high success rates. This is due to the compact arrangement of the plexus at this level. The location of such large amount of innervation in such reduced area does not have a parallel in the lower extremity or anywhere else for that matter, qualifying the supraclavicular block as the most successful plexus block in the whole body. Indeed it has been called the spinal of the upper extremity. Because of reports of pneumothorax supraclavicular block started to lose its appeal in the 1950 s. By the 1960 s most of practitioners started to favor the axillary block. A rational approach should have been to deal with the pneumothorax issue by finding reliable superficial landmarks for the dome of the pleura. An anatomical approach that relies first on establishing the pleura boundaries is the technique we perform and it is the reason we have made this block much safer. This allows us to take advantage of such extraordinary block while limiting its potential drawbacks. Our experience to late 2005 includes more than three thousand supraclavicular techniques without any pneumothorax being demonstrated. A common question posed to us is whether we perform routine chest X-rays after a supraclavicular block. The fact is that we only do an X-ray when the clinical situation calls for it (e.g., an unusually difficult technique). The literature predominantly shows that when a pneumothorax associated with a supraclavicular technique has been found it has been after the patient developed clinical symptoms and not because of routine chest x-ray post block. So our practice of performing selective chest X-rays as necessary is comparable to the common practice in the rest of the country. Some history of the supraclavicular technique The supraclavicular block was introduced into clinical practice in Germany by Kulenkampff in 1911 and a publication of his technique appeared later in the English literature in Kulenkampff accurately described the plexus as being more compacted in the neighborhood of the subclavian artery where he believed a single injection could suffice to provide adequate anesthesia of the entire upper extremity. Kulenkampff s technique was simple and in many ways sound. Unfortunately his recommendation to introduce the needle toward the first rib in the direction of the spinous process of T2 or T3 carried an inherited risk for pneumothorax. 68

69 Albeit with several modifications, the supraclavicular block remained a popular choice until the early 1960 s. Eventually, the combined effect of pneumothorax risk and the introduction of the axillary approach by Accardo and Adriani in 1949 and especially by Burnham in 1958 marked the beginning of the decline for one of the best regional anesthesia techniques ever described. The axillary approach introduced a good technique with its share of shortcomings (e.g., smaller area of anesthesia than supraclavicular, tendency to produce patchy blocks and lower overall success rate) but definitely devoid of pneumothorax risk. The axillary block received a big push when in 1961 De Jong published an article in Anesthesiology praising it. The paper was based on cadaver dissections and included the now famous calculation of 42 ml as the volume needed to fill a cylinder 6 cm long, that according to De Jong should be sufficient to completely bathe all branches of the brachial plexus. Coincidentally (or not) the same journal carried a paper by Brand and Papper out of New York, comparing axillary and supraclavicular techniques. This article is the source of the 6.1% pneumothorax rate frequently quoted for supraclavicular block. In retrospect these two articles could be considered the point at which the tide definitely turned against the supraclavicular block making the axillary route the most common approach to the brachial plexus in the United States and the rest of the world. With some exceptions this is still true today. Some authors also cite the perceived complexity of supraclavicular block as the reason for not performing it more often. However the advantages of a supraclavicular technique, namely its rapid onset, density, high success rate along with large area of anesthesia are too good to ignore. These good characteristics are, according to David Brown and colleagues, unrivaled by other techniques. In our practice the supraclavicular approach is the cornerstone of upper extremity regional anesthesia. Patient position and landmarks The patient lies supine with the head of the bed elevated 30 degrees (fig 6.5). The ipsilateral shoulder is down and the head is turned to the opposite side. The arm to be blocked is flexed at the elbow and if possible the wrist is supinated so that a twitch of the fingers can be easily detected. We use the same position for ultrasound-guided technique. Fig 6-5. Patient position. The patient lies supine with the head of the bed elevated 30 degrees. The head of the patient is turned, the shoulder is down and the arm is flexed at the elbow and supinated at the wrist. (On a model with permission). 69

70 The point at which the clavicular head of the SCM muscle inserts in the clavicle is then identified as shown in fig 6-6. A parasagital (parallel to the midline) plane that crosses this point determines an unsafe zone medial to it, where the risk of pneumothorax is high and a lateral zone that is safer. Fig 6-6. Lateral head of SCM. The lateral (clavicular) head of the SCM at its junction with the clavicle is marked with an arrow. Medial to this plane the risk of pneumothorax increases. (On a model with permission). Because the trunks are short and run in a very steep direction caudally towards the clavicle, there is a narrow window of opportunity to perform the block above the clavicle. It must be performed at enough distance from the insertion of the clavicular head to make it safe from pleural invasion, and close enough to this point to still reach the trunks before they disappear behind the clavicle. We call this distance the safety margin. In adults we calculate this distance to be about 1 inch (2.5 cm), which corresponds to the width of the author s thumb. This distance is marked on the skin over the clavicle for orientation as shown in figure 6-7. Fig 6-7. Safety margin A safety margin of 1 lateral to the lateral insertion of the SCM is marked over the clavicle. (On a model with permission). This is only an orientation point because the actual point of needle entrance is determined by palpation of the most lateral elements of the plexus in the supraclavicular area immediately above the orientation point. At this level the brachial plexus is usually easily palpable either as a groove or some type of cord. This is usually called interscalene groove but the interscalene groove only exists high in the C5-C6 level. The palpating finger is placed parallel to the clavicle and the point of needle entrance is marked with a downward pointing arrow as shown in figure 6-8 (upper lateral 70

71 arrow). Over the clavicle an upward pointing arrow is also drawn as shown in figure 6-8 (lower lateral arrow). Both arrows together show the direction of the needle, which is parallel to the midline. The lower lateral arrow also marks the caudal limit for penetration of the needle (as far caudal as we are willing to go), keeping it supraclavicular and away from the first intercostal space. Fig 6-8. Orientation arrows. The medial arrow (pointing up) shows the most lateral boundary of the pleura. The upper lateral arrow shows the needle entrance point, the lower lateral arrow indicates the caudal limit for needle penetration. The two opposing lateral arrows (one up, one down) show the needle trajectory (parallel to the midline of the patient). (On a model with permission). Nerve stimulator technique The needle is inserted first anteroposterior (perpendicular to the skin) for a distance of a few mm up to 1.5 cm depending on the amount of subcutaneous tissue present as shown in figure 6-9. Usually a twitch of the upper trunk (shoulder) is found as evidence that the needle is approaching the plane of the plexus. Fig 6-9. Direction of the needle The needle is first introduced perpendicular to the skin. (On a model with permission). The direction of the needle is then changed to caudal advancing it now parallel to the midline (and parallel to the most lateral pleural boundary), as shown in figure Fig Direction of the needle And then advanced caudal parallel to the midline (On a model with permission). 71

72 The reference to the midline is easy to ascertain and avoids the use of other landmarks (e.g., nipple), which have enormous patient-to-patient variability. The needle is advanced caudally with a slight posterior angle. Because the trunks are physically contiguous a twitch of the upper trunk (shoulder) is followed by middle trunk (pectoralis, triceps, supination, pronation) and finally lower trunk (wrist and fingers). The goal of the technique is to stimulate the fingers. Wrist flexion and extension are acceptable responses but supination or pronation and other more proximal twitches are not. If advancing the needle after finding a twitch of the upper or middle trunk makes the twitch disappear it means that the angle of the needle is not matching the orientation of the trunks and that the tip of the needle is wandering away from the trunks. The needle is slowly withdrawn until the original twitch is once again visible and then redirected either posteriorly (most of the times) or anteriorly but always parallel to the midline. It is very important not to advance the needle more than 2 cm in the caudal direction if no twitch is visible. In this case the situation is reassessed starting with the nerve stimulator and its connections. As long as a twitch is being elicited the needle can be safely advanced caudally without regard to depth. Ultrasound technique We also use the semi sitting position. A linear probe as for the interscalene block is used. We usually start scanning high in the neck at above C6 to identify SCM, scalene muscles and great vessels. The probe is then advanced caudally and placed just above the clavicle. The angle (tilting) is adjusted to get a good cross section of the subclavian artery and the scalene muscles. The plexus, either trunks or the divisions are visualized behind and proximal to the artery in a characteristic honeycomb arrangement. The needle is directed in plane from lateral to medial under the probe. The needle should be inserted at 1-2 cm away from the probe to avoid a steep angle of insertion that would make its visualization harder. The needle is directed toward the lower trunk in the proximity of the subclavian artery. The anesthetic solution should be seen surrounding the plexus. Local anesthetic and volume For single shot techniques in adults, 30 ml to 40 ml of 1.5% mepivacaine plain will provide 2-3 h of anesthesia. The addition of 1:400,000 epinephrine prolongs the anesthesia to about 3-4 h. The residual analgesia post anesthesia is variable in duration although rarely persists for more than 2 h after block resolution. Ropivacaine 0.5%- 0.75% can be used in the same volume to provide 4-7 h of anesthesia. The addition of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine accomplishes similar extended duration with shorter onset, although the onset is longer than for mepivacaine alone. Also ml of 0.2% ropivacaine can be used to provide postoperative analgesia for surgery performed under general anesthesia. Complications Besides the common complications accompanying any block, the supraclavicular technique can also be followed by Horner s syndrome, hoarseness and phrenic nerve 72

73 palsy, but less frequently than after interscalene block. Neal et al in 1998 studied diaphragmatic paralysis in 8 volunteers after supraclavicular block using ultrasound (replicating what Urmey et al did in 1991 to demonstrate 100% of diaphragmatic paralysis after interscalene block). They found an incidence of 50% of diaphragmatic paralysis. No subject experienced changes in pulmonary function tests (PFT) values or subjective symptoms of respiratory difficulty. This is our experience too. Clinical pearls This is not a block for a practitioner that rarely performs peripheral nerve blocks. The person interested in learning to perform it should first become familiar with the anatomy of the supraclavicular area including the dome of the pleura. Using ultrasound makes the visualization of the pleura easier, but still requires the operator to be familiar with the anatomy of the area. The block should not be attempted unless the insertion of the sternocleidomastoid in the clavicle is clearly established. In fact this is a must especially for a person not experienced with the technique. With time it becomes easier to ascertain the boundaries of the SCM. It helps to know that the neurovascular bundle crosses the clavicle under the midpoint of it, so this should be kept in mind as a reliable reference. Due to the steep direction of the plexus from the neck to the axilla, the higher in the neck (the further away from the clavicle) the more medial the plexus is. By the same token, the further below the clavicle the more lateral to its midpoint the plexus is. The needle should never be inserted more than 2 cm caudal if no twitch is elicited. This warning applies to every patient regardless of weight. The injection should always be slow alternated with frequent aspirations, this gives time to recognize accidental intravascular injection in those cases where blood is not aspirated. I also believe it helps to keep the needle from moving backwards as a result of high speed flow at the tip of the needle. 73

74 INFRACLAVICULAR BLOCK Indications This block is more suited for surgery distal to the elbow. Point of contact of the needle with the brachial plexus The needle approaches the plexus at the level of the cords in the proximity of the terminal branches. Main characteristics The infraclavicular block is really an axillary block in which the needle enters the axilla through its anterior wall (pectoralis muscles) instead of through its base. This fact is usually unrecognized and infraclavicular block is presented as a block completely different than axillary. It is a good place to place a catheter since it is less mobile than neck and axilla. It also hurts more because is a deep block that requires the needle to go through muscle. Patients should be adequately sedated. It is widely recommended to obtain a distal twitch in the hand or wrist and to avoid a biceps twitch (musculocutaneous nerve or lateral cord) or pronation of the forearm (lateral cord). This is based on clinical experience. I believe that when the needle approaches the plexus at the level of the cords there is no clear rationale to prefer one cord to the other, although musculocutaneous stimulation could come form stimulation of this nerve lateral to the main bundle. I any, it is theoretically possible that a twitch from the posterior cord (elbow, wrist and or finger extension) could be better because the posterior cord is located at about the same distance from the other two, and subjected to more pressure from outside, although it is more difficult to get to it. Many infraclavicular techniques have been described. A simple technique is the coracoid approach first described by Whiffler in the British Journal of Anaesthesia in 1981 and later redefined by MRI studies performed in volunteers (20 males and 20 females) by Wilson, Brown et al and published in Regional Anesthesia in Patient position and landmarks The patient lies supine with the ipsilateral shoulder down. The coracoid process is found by palpation and marked on the skin. It is located below the clavicle (around 2 cm) at the level of the deltopectoral sulcus at the junction of the middle third with the lateral third of the clavicle. A C-arm X-ray machine can be useful if available. The point of needle entrance is marked 2 cm caudal and 2 cm medial to the coracoid process as shown in fig Fig Needle entrance point. Two cm caudal and two cm medial from the coracoid process. (On a model with permission). 74

75 Nerve stimulator technique The nerve stimulator is set to deliver a current of ma at a frequency of 1 Hz and 0.1 ms of pulse duration. It is frequently necessary to use a 4 (10 cm) needle to be able to reach the plexus. The needle attached to the nerve stimulator is advanced in the anteroposterior direction, perpendicular to the skin, as shown in figure Fig Direction of the needle The needle is introduced perpendicular to the skin. (On a model with permission). Before entering in contact with the plexus the needle passes through the pectoralis major and pectoralis minor muscles producing a visible local twitch. Deep to them the plexus is found. If not response from the plexus is obtained the needle is redirected caudal (most of the time) or cephalad but in the same parasagital plane without medial or lateral deviation. Ultrasound technique Because the brachial plexus is deeper at this level under pectoralis major and minor muscles a linear probe with lower frequency is usually used in the range of 4-7 MHz. The probe is aligned almost perpendicular to the junction between the middle and lateral thirds of the clavicle in the proximity of the coracoid process. This way a cross section of the plexus and axillary vessels is obtained. The tilt is adjusted until a clear view in cross section comes to view. The needle can be advanced in plane with the probe from proximal to distal or vice versa and the best target, if a single injection is desired, is the posterior cord behind the artery. Separate injections of the cords can be done as needed. Local anesthetic and volume This block requires a higher volume for better results. Usually ml of 1.5% plain mepivacaine will provide 2-3 h of anesthesia. The addition of 1:400,000 epinephrine prolongs the anesthesia to about 3-4 h. The residual analgesia post anesthesia is variable in duration although rarely persists for more than 2 h after block resolution. Ropivacaine 0.5% can be used in the same volume to provide 4-6 h of anesthesia. The addition of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine accomplishes similar extended duration with shorter onset, although the onset is longer than for mepivacaine alone. Also 30 to 40 ml of 0.2% ropivacaine can be used to provide postoperative analgesia for surgery performed under general anesthesia. 75

76 Complications Pneumothorax can occur due to injury of the pleura through an intercostal space. Muscle pain and hematomas, which can be large in size, are not uncommon. Clinical pearls This is a good place to put a catheter because it is easier to fix it. Use adequate sedation, as this block is more uncomfortable for patients. The block should not be attempted medial to the junction between the lateral third and middle third of the clavicle because of increased risk of pneumothorax. 76

77 AXILLARY BLOCK Indications It is best suited for surgery distal to the elbow. Point of contact of the needle with the brachial plexus The needle approaches the plexus at the level of its terminal branches. Main characteristics The axillary block is not properly a plexus block, but rather a block of the terminal branches of the brachial plexus. The distance between the different branches plus the expanding wave of the axillary artery pulse are obstacles that the local anesthetic must overcome to adequately reach the nerves. A single injection technique is an option, but a second and even a third injection have shown to increase the success rate. If a single injection is to be attempted, the epicenter of the injection if possible, has to coincide with the specific nerve responsible for the sensory innervation of the surgical area. For example, to deal with an extensor tendon injury of the thumb (radial nerve) the injection should occur around the radial nerve. The same is true for lesions located in the ulnar and median territories. If the surgical area involves more than one terminal nerve, the single injection technique should be performed in the proximity of the radial level because I believe the solution diffuses more easily from back to front that vice versa. This may be because of more resistance in the back of the plexus (muscles and scapula) than in front (subcutaneous tissue). The anatomy lab also shows that better diffusion could be obtained by placing a pillow under the elbow with the shoulder abducted slightly less than 90 degrees. A point usually stressed in the literature is to perform the block as proximal in the axilla as possible. This can be uncomfortable to the patient and challenging to the anesthesiologist. The only perceived advantage would be to increase the chances of blocking the musculocutaneous nerve before it leaves the plexus. This is never certain. A better strategy is to block this nerve first before performing the block of the rest of terminal branches. Although some variability exists, usually the median nerve is superficial (anterior) to the artery following its same direction, the ulnar nerve (and medial brachial/antebrachial cutaneous) are medial and somewhat posterior to the artery, the musculocutaneous nerve is lateral to the artery (and eventually under the biceps muscle) and the radial nerve is posterior to the artery. Patient position and landmarks I do not like the transarterial technique so we will only discussed nerve stimulator and ultrasound techniques. The patient is supine, the arm is abducted to about 80 degrees and the elbow is elevated 30 degrees by using a small pillow or folded blanket. The biceps muscle is identified by visualization and/or palpation, under which a cord like structure signals the presence of the coracobrachialis muscle. Immediately posterior to it the pulse of the axillary artery can be found. A marker is used to identify the proximal trajectory of the artery in the upper arm/axilla junction. See figure

78 Fig The arm is abducted about 80, the elbow is elevated slightly with a small pillow and the axillary artery is marked. (On a model with permission). Nerve stimulator technique A 2, 22-gauge insulated needle usually suffices. The block of the musculocutaneous nerve is accomplished first. The operator identifies and holds the patient s biceps muscle with one hand and directs the needle with the other in a direction perpendicular to the main axis of the arm into the substance of the choracobrachialis muscle as shown in fig Fig Blocking the musculocutaneous nerve. The needle is introduced under the biceps perpendicular to the main axis of the arm. (On a model with permission). At some point under the biceps a motor twitch of the elbow in flexion is elicited. The current is reduced to 0.5 ma and 5 ml of local anesthetic solution is slowly given. The needle is then withdrawn and the nerve stimulator is set again to ma. Using the mark of the axillary artery on the skin as a reference, the needle is directed either tangential to it (median), medial to it (ulnar and medial brachial/antebrachial) or posterior to it (radial), see figure Fig The needle is introduced in reference to the axillary artery using the mark on the skin without the need to feel for the pulse again. (On a model with permission). 78

79 Ultrasound technique The brachial plexus once again is superficial here so a linear probe with a frequency of MHz is commonly used. The arm is abducted and a pillow is placed under the elbow just as described for the nerve stimulator technique. The probe is placed across the neurovascular bundle to get an image of it in cross section. The median nerve is usually seen superficial (anterior) to the artery. The ulnar is medial and somewhat posterior, the radial is posterior. Distally in the axilla the radial nerve starts shifting more lateral but it still remains posterior to the artery. The musculocutaneous is lateral to the artery at all times and it can be seen entering the coracobrachialis muscle. If a single injection is planned it should be made in the proximity of the radial nerve. Individual injections of terminal nerves can be done as needed. Local anesthetic and volume The terminal nerves in the axilla are more separated than at more proximal locations. The terminal branches of the plexus are enclosed in a fibrous sheath which is filled with loose connective tissue. This connective tissue-and no septa- is an obstacle to the free diffusion of local anesthetic within the sheath. In addition, the pulsatile force of the axillary artery, located at the center of the neurovascular bundle, most likely helps promote longitudinal spread of local anesthetic as opposed to circumferential spread. For these reasons an axillary block should be performed using a higher anesthetic volume than at other more proximal locations, 50 ml and even 60 ml injected slowly using the usual precautions is the volume most used. A multi injection technique is a justifiable alternative. Complications Pneumothorax is virtually impossible to get from this location. Hematomas from vascular puncture are more common and can be associated with nerve damage. Pearls This is a block mainly indicted for surgery on the distal forearm, wrist and hand. It is not a good choice for elbow surgery. Tourniquet pain is an issue and not necessarily due to intercostobrachial nerve, but mainly due to insufficient proximal anesthesia of the whole arm. The main injection should aim for the nerve most responsible for the sensory innervation of the surgical site. 79

80 References 1. Brown DL. Brachial plexus anesthesia: an analysis of options. Yale J Biol Med 1993; 66: Franco CD, Vieira Z. 1,001 subclavian perivascular brachial plexus blocks: success with a nerve stimulator. Reg Anesth Pain Med 2000; 25: Franco CD. The subclavian perivascular block. Tech Reg Anesth Pain Med 1999; 3: De Andres J, Sala-Blanch X. Peripheral nerve stimulation in the practice of brachial plexus anesthesia: a review. Reg Anesth Pain Med 2001; 26: Greenblatt Gm, Denson GS. Needle nerve stimulator-locator: nerve blocks with a new instrument for locating nerves. Anesth Analg 1962; 41: Hadzic A, Vloka J, Hadzic N, et al. Nerve stimulators used for peripheral nerve blocks vary in their electrical characteristics. Anesthesiology 2003; 98: Brown DL. Atlas of regional anesthesia. Philadelphia, PA: W.B. Saunders, Mulroy MF. Regional anesthesia: An illustrated procedural guide. 3 rd edition. Philadelphia, PA; Lippincott Williams & Wilkins Franco CD, Domashevich V, Voronov G, Rafizad A, Jelev T. The supraclavicular block with a nerve stimulator: To decrease or not to decrease, that is the question. Anesth Analg 2004; 98: Neal JM, Hebl JR, Gerancher JC, Hogan QH. Brachial plexus anesthesia: Essentials of our current understanding. Reg Anesth Pain Med 2002; 27: Perlas A, Chan V: Ultrasound-assisted nerve blocks. In: Textbook of Regional Anesthesia, Hadzic A, ed. New York, McGraw Hill, 2007, pp

81 CHAPTER 7 LOWER EXTREMITY NERVE BLOCKS Anatomy 82 Subgluteal fold..85 Male and female pelvis issue 85 Lateral femoral cutaneous nerve block.86 Femoral block 87 Obturator nerve block 89 Lumbar plexus block.90 Sciatic nerve block, classic (Labat-Winnie)..92 Sciatic nerve block, Franco s...94 Sciatic subgluteal nerve block, di Benedetto s..97 Sciatic subgluteal nerve block, Franco s...99 Popliteal nerve block, Franco s Popliteal nerve block, lateral approach References

82 LOWER EXTREMITY BLOCKS The innervation of the lower extremity comes from the lumbar and sacral plexuses. It is important to realize that the different nerve elements of the lower extremity run more separated from each other than in the upper extremity and that they are never confined to a small surface area like it happens at the level of the trunks of the brachial plexus. The fact that no single peripheral block technique can provide anesthesia of the whole lower extremity and the high success of neuraxial anesthesia have contributed to make lower extremity peripheral nerve blocks less popular than the techniques of the upper extremity. The introduction of low molecular weight heparins with their increased risk for epidural hematoma has produced a renew interest in lower extremity nerve blocks. Anatomy Lateral femoral cutaneous nerve It is an exclusively sensory nerve originating form L2-L3 roots. It appears in the pelvis lateral to the psoas muscle, caudal to the ilioinguinal nerve. Its course is anterolateral, under the iliac fascia, parallel to the iliac crest. It emerges from the pelvis under the inguinal ligament between the anterior superior and anterior inferior iliac spines to provide sensory innervation of the lateral thigh. Femoral nerve It is a motor and sensory nerve derived from the posterior divisions of L2-L3-L4 roots. It is also located in the pelvis lateral to the psoas muscle in the cleavage between the psoas and the iliacus muscle. As it passes under the inguinal ligament the nerve runs superficial to the iliopsoas muscle. Approximately 3-4 cm below the inguinal ligament, the femoral nerve divides into anterior and posterior divisions. The anterior division has two sensory branches supplying the anteromedial thigh and two muscular branches supplying the sartorius and pectineus muscles. The posterior division has one sensory branch, the saphenous nerve, and muscular branches to the quadriceps. At it passes under the inguinal ligament the femoral nerve has the femoral artery medial to it while the femoral vein is medial to the artery (VAN from medial to lateral). The nerve is covered by the iliac fascia, which separates it from the vascular structures, and more superficially by the deep fascia of the thigh (fascia lata). The muscular branch to the rectus femoris also supplies the hip joint and the muscular branches to the three vasti muscles also supply the knee joint. Obturator nerve It is usually a mixed nerve (motor and sensory) derived from the anterior divisions of L2-L3-L4 roots. It enters the pelvis on the medial side of the psoas muscle, courses anteriorly along the lateral pelvis until reaching the obturator foramen. After entering the thigh the nerve divides into anterior and posterior branches. The anterior division runs downwards in front of the obturator externus and the adductor brevis and behind the pectineus and adductor longus. It gives innervation to the gracilis, adductor brevis and adductor longus and sometimes to the pectineus. It gives also articular branches to the hip joint. On occasions it supplies the skin of the medial side of the thigh. 82

83 The posterior division pierces the obturator externus and passes downwards behind the adductor brevis and in front of the adductor magnus. It supplies the obturator externus, the adductor magnus and the knee joint. The anterior sensory branch can be frequently missing and in that case the medial thigh is also supplied by the femoral nerve. The highly variable distribution of the sensory branch of the obturator nerve has contributed to the confusion about how much can be obtained by a single block performed at the femoral level ( 3-in-1 block). Sciatic nerve It is the largest nerve in the body. It originates from L4-L5, S1-S3 roots (part of the anterior ramus of L4 joins the anterior ramus of L5 to originate the lumbosacral trunk which together with the first three sacral roots forms the sciatic nerve). The nerve has two components, the tibial nerve (medial side of the nerve), which is derived from the anterior divisions of L4-L5, S1-S3 and the common peroneal nerve (on the lateral side), which is derived from the posterior divisions of L4-L5, S1-S2. These two components can be easily identified as two separate nerves in about 11% of the cases, but even in those cases the two components are surrounded by a common sheath. Thus this early division, as it is erroneously called, has no clinical significance. The nerve comes out of the pelvis through the greater sciatic foramen and enters the gluteal region anterior to the piriformis muscle, cephalad to the ischium. After clearing this bone structure it turns vertically downwards to pass in between the ischium medially and the greater trochanter laterally, as shown in figure 7.1. The sciatic nerve from about mid-gluteal level to the subgluteal fold follows a parallel trajectory to the midline at a distance of about 10 cm in adult patients. With the hips in adduction this distance is maintained throughout adult life and it is NOT influenced by gender or body weight. This previously unknown fact has simplified enormously the approach to the sciatic nerve in our practice. Fig 7-1. The sciatic nerve (1) travel parallel to the midline (5). Piriformis muscle (2), ischium (3) and greater trochanter (4) are also shown. (Own dissection). The nerve enters the thigh deep to the biceps femoris muscle. In the thigh, the position of the nerve with respect to the midline is influenced both by the degree of hip abduction as well as by the amount of fat accumulating in the inner thigh. At the apex of the popliteal fossa the two nerve components, peroneal and tibial, finally divert from each other having never mixed their fibers. The posterior tibial nerve continues in the direction of the main trunk at the center of the fossa. The common peroneal turns lateral and runs just medial to the biceps tendon. 83

84 Subgluteal fold The fold under the buttocks is a fold of the skin and does not corresponds with the lower border of the gluteus maximus muscle as frequently thought. In fact the inferior border of this muscle crosses the subgluteal fold diagonally and extends further caudal as the muscle inserts laterally in the iliotibial tract (see figure 7-2). So if a subgluteal approach to the sciatic nerve is attempted instead of a mid-gluteal, the needle crosses a thinner layer of fat but still passes through the gluteus maximus. Anesthesia of the posterior cutaneous nerve of the thigh is not reliable at this level because this nerve usually is already superficial (above the fascia) at the subgluteal fold. Fig 7-2. The inferior border of the gluteus maximus and subgluteal fold are two different things. They cross each other diagonally. (Own dissection). Genitofemoral nerve It derives from L1-L2 roots and provides some innervation of the genital area and the medial proximal area of the thigh over the femoral vessels. Posterior cutaneous nerve of the thigh Also known as posterior femoral cutaneous nerve. It is not a branch of the sciatic nerve, although it has a close relationship with it in the gluteal area before it separates from it to become a superficial nerve. It is derived from S1-S3 and exits the pelvis through the greater sciatic foramen first medial and then superficial (more posterior in anatomic position) to the sciatic nerve. Somewhere caudal to the ischium, the nerve pierces the deep fascia (fascia lata) and becomes a superficial structure. It innervates the skin over the lower part of the buttocks as well as the posterior thigh and frequently extends toward the proximal posterior leg. A block of the sciatic nerve performed proximally in the gluteal area will predictably produce anesthesia of this cutaneous nerve as well. A block performed at the subgluteal level will not reliably block it. Saphenous nerve It is a sensory nerve that originates from the posterior division of the femoral nerve in the inguinal region. It runs down along with the femoral vessels under the cover of the sartorius muscle. It emerges on the medial side of the knee between the tendons of sartorius and gracilis and at one point caudal to the knee it pierces the deep fascia to become superficial. Below the knee it gives off the subpatellar branch, which supplies the medial side of the knee (chance for injury during knee arthroscopy). As it becomes 84

85 superficial it joins the greater saphenous vein in the leg running alongside it to pass in front of the medial malleolus and finish at about the base of the first metatarsal. Male and female pelvis issue The pelvis of the female is adapted to accommodate child bearing and as a result the female inner pelvis is wider than males. However, the total width of the bony pelvis, that is the diameter between both iliac crests (bicrestal diameter), is similar in both sexes, 280 mm in males and 275 mm in females in average. The thicker bones in the male pelvis compensate for a roomier female pelvis. According to the anthropologists (3) the human bony pelvis is surprisingly similar in males and females at all ages. The difference in pelvis size corresponds to hormone-dependent different patterns of fat deposition in both sexes. In other words the difference in pelvic size among the sexes is mostly due to soft tissue and not bony pelvis. The bony pelvis determines the position of the sciatic nerve in the buttocks. Clinical pearls The nerves of the lower extremity are distant from each other. The position of the sciatic nerve in the buttocks with respect to the midline is not affected by gender or obesity. Its relationship to bone structures and to the midline remains unchanged throughout adulthood. The inferior border of the gluteus maximus muscle does not correspond with the subgluteal fold (Snell s Clinical Anatomy for Medical Students, 3 rd edition, page 554). In fact both cross each other diagonally. The subgluteal fold is a fold of the skin anchored to the deep fascia. The inferior border of the gluteus maximus muscle goes diagonally from medial to lateral to insert in the iliotibial tract. The gluteus maximus is the only gluteal muscle to cover the sciatic nerve superficially caudal to the piriformis muscle. Gluteus medius and minimus are located cephalad and lateral to the sciatic nerve. The inguinal crease does not correspond deep with the inguinal ligament. Both structures are parallel to each other. The inguinal crease runs about 1 inch (2.5 cm) caudal and parallel to the inguinal ligament. 85

86 LATERAL FEMORAL CUTANEOUS NERVE BLOCK Indications This block can be performed alone to provide anesthesia of the lateral thigh for the donor area of a skin graft. It can also be performed along with femoral, obturator and sciatic blocks to provide anesthesia of the thigh for some above the knee procedures and thigh tourniquet. It is one of the nerves potentially blocked with a 3-in-1 block, a block of the femoral nerve performed with a higher volume of local anesthetic that aims to block the lateral femoral and obturator nerves as well (not supported by the evidence). Point of contact with the nerve The nerve is approached as it emerges from under the inguinal ligament, medially and inferior to the anterior superior iliac spine (ASIS). Main characteristics This can be a superficial block (above the fascia lata) if the block is performed a couple of cm or more below the inguinal ligament. More proximally the nerve is under the fascia lata. This is important because this fascia is thick enough to slow the transfer of local anesthetic to the target nerve. Patient position and landmarks The patient lies supine. The ASIS is identified by palpation. Technique The needle entrance point is identified about 1 cm medial and 1 cm caudal to the ASIS. The needle is advanced perpendicular to the skin and directed deep to the fascia where the local anesthetic is injected in a fanwise fashion. A nerve stimulator with pulse duration of 0.3 to 1 ms (300 to 1000 µsec) can be used to elicit a paresthesia in the lateral thigh. Local anesthetic and volume A volume of 5 to 10 ml of 1% mepivacaine is frequently used. A long acting agent can be used if necessary. Complications Very rare. Some patients can complain of dysesthesia in the area from minor injury to the nerve. It usually goes away without sequelae. 86

87 FEMORAL NERVE BLOCK Indications An isolated femoral nerve block can be performed to provide anesthesia for surgery on the anterior thigh, patella and some knee procedures. It is more commonly performed along with sciatic to provide anesthesia of the entire lower extremity. Point of contact with the nerve The nerve is approached just below the inguinal crease (about 1 inch distal to the inguinal ligament) lateral to the femoral artery. Main characteristics This is a simple block performed lateral to the pulse of the femoral artery, deep to the fascia lata (deep fascia of the thigh) and deep to the fascia iliaca (the fascia that covers the iliopsoas muscle). The femoral artery pulse usually provides an easy and reliable landmark to the nerve. Ultrasound provides a good image of the nerve and neighboring vascular structures facilitating any technique to block it. Patient position and landmarks The patient lies supine. If necessary the back of the bed can be elevated for patient s comfort. If done in combination with a sciatic nerve block, we prefer to do the sciatic block first because this is a block that needs more time to settle than the femoral. The femoral pulse at the inguinal crease is recognized and the trajectory of the artery is marked. The point of entrance is marked on the skin just below the inguinal crease at about 2 cm lateral to the pulse. Nerve stimulator technique A 2, insulated needle usually suffices. The nerve stimulator is set at 1.0 ma, a frequency of 1 Hz and pulse duration of 0.1 msec (100 µsec). The needle is directed 45- degree cephalad and parallel to the femoral artery in the direction of the inguinal ligament. A twitch of the quadriceps muscle with movement of the patella is a good response. The current is lowered to about 0.5 ma or less and if the response is still visible a slow injection is started. A response from the sartorius is usually considered not a good response because it could become from stimulation of the nerve to the sartorius, a branch of the anterior division of the femoral nerve. My own anatomic dissections fail to make the case for this precaution because the point at which the block is attempted is usually cephalad to any separation of the branch to the sartorius from the main nerve. Ultrasound technique The femoral nerve is relatively superficial in many patients. As usual use a high frequency probe (>10 MHz) to define structures expected to be at less than 3 cm of depth. For deeper structures use less than 10 MHz of frequency, which provides deeper penetration and less resolution. A linear probe at MHz can usually provide a good image of the femoral nerve and vessels. The probe is placed on top of the inguinal crease if the needle is going to be advanced out of plane with the image of nerve in cross section. The probe can be placed immediately below the inguinal crease if the needle will be advanced in plane with 87

88 the probe from lateral to medial. The femoral vein is the most medial structure of the neurovascular bundle and is easily collapsible by the probe. The artery is just lateral to it. The nerve is lateral to the artery with usually a gap of about 1 cm in between. The image obtained is in cross section. Local anesthetic and volume A slow injection of 20 ml of 1% or 1.5% mepivacaine is usually used for this block. The use of a bigger volume in an attempt to produce a 3-in-1 block by cephalad spread of local anesthetic lacks support in the literature. Complications Very rare. Hematomas from puncture of the femoral artery are possible but avoidable with meticulous technique, use of small gauge needles and thorough compression of the arterial puncture when it occurs. The use of ultrasound almost eliminates this problem. 88

89 OBTURATOR NERVE BLOCK Indications It is most commonly combined with femoral, lateral femoral and/or sciatic blocks. Point of contact with the nerve The needle approaches the nerve after it exits the obturator foramen below the inguinal ligament. Main characteristics This is a deep block that requires good anatomical knowledge. Patient position and landmarks The patient lies supine. The easiest way to do it is to use the femoral artery pulse at the inguinal ligament as the main landmark. The point of needle entrance is found about 4 cm medial to the artery and 2 cm below the inguinal crease. Technique A 4, insulated needle connected to a nerve stimulator is advanced perpendicular to the frontal plane. A local twitch from the pectineus and or adductor longus is usually obtained. This is just a direct muscle twitch. Deep to this level the tip of the needle reaches the nerve and produces thigh adduction. The current is lowered to 0.5 ma and if a twitch is still visible a slow injection is started. If the needle makes contact with the pubis ramus it is walked off caudally. Local anesthetic and volume Usually ml of 1% to 1.5% mepivacaine or a longer acting agent is used. Complications Hematoma is the most frequent complication of this technique. 89

90 LUMBAR PLEXUS BLOCK (alternatively called psoas compartment block ) Indications Its goal is to produce anesthesia of the lateral femoral, femoral and obturator nerves, so it can be used along with sciatic nerve to provide anesthesia of the entire lower extremity. It is also used to provide postoperative analgesia after hip and knee surgery. Point of contact with the nerve(s) The plexus is accessed deeply in the lumbar area in the space between the quadratus lumborum posteriorly and the psoas muscle anteriorly. Main characteristics It is the posterior approach to a 3-in-1 block. It is a deep block in which the needle must traverse the mass of paraspinal muscles, go through the quadratus lumborum muscle to end in the space between the latter and the psoas muscle in the retroperitoneal space. Because of the depth at which the nerves are located, the operator has little control over the exact location of the tip of the highly flexible needle, increasing the potential risk for complications. It is essential that the operator be familiar with the anatomy. The epidural, subdural and intrathecal spaces are very close to the trajectory of the needle and so are the kidneys and the iliac vessels. Cases of penetration of the peritoneal cavity with injury of the contents have been reported. This block should not be performed in obese patients. Patient position and landmarks The patient is placed in the lateral position with both hips and knees flexed like for neuraxial block. A line joining both iliac crests is drawn (L4-L5 interspace). The posterior superior iliac spine is identified and a line passing at this level is drawn perpendicular to the first line. The point of intersection is the entrance point. Alternatively the point of entrance can be found at 4-5 cm from the midline at the crestal line. Nerve stimulator technique A 4, insulated needle connected to a nerve stimulator is used. The needle is advanced parallel to the midline, perpendicular to the skin. If the transverse process of L4 is contacted the needle is walked off caudally. A muscle twitch of the femoral nerve or obturator indicates good placement. It is frequent to accept higher currents (around 1 ma) to inject. Thorough aspiration for blood or CSF is performed combined with slow injection alternated with frequent aspirations. Ultrasound technique This is a deep block. Some people use a curved 4-5 MHz probe to delineate the psoas and the anatomy of the lumbar plexus but it is more challenging. We do not perform it routinely. 90

91 Local anesthetic and volume A volume of ml of 1% mepivacaine or 0.5% ropivacaine can be used. For analgesia the concentration is halved. Complications This is the regional anesthesia technique associated with the highest amount of complications. Retroperitoneal hematomas, subdural and intrathecal injection with development of total spinal, as well as kidney and bowel punctures have been reported. Clinical pearls This is a deep block with important potential complications like subdural and intrathecal injection and development of total spinal. Great vessel puncture with retroperitoneal hematoma as well as kidney and intra abdominal viscera injury have been reported. The anesthesiologist must carefully balance the potential benefits against the risks of complications. 91

92 SCIATIC NERVE BLOCK Classic approach (Labat as modified by Winnie) Indications Alone it provides anesthesia of the back of the thigh (through anesthesia of the posterior cutaneous nerve of the thigh, a branch of the sacral plexus) and most of the lower extremity below the knee with the exception of the medial side of the leg (saphenous nerve). If used along with femoral, lateral femoral and obturator nerve blocks it produces anesthesia of the entire lower extremity. Point of contact with the nerve The nerve is contacted at the point where it is curving downwards as it emerges caudal to the piriformis muscle. The needle on occasions could also traverse through the piriformis. Main characteristics Labat s approach is a highly anatomic approach that requires the identification of the anterior superior iliac spine (ASIS) and the greater trochanter (GT). A dissection of the gluteal area shows that this is an accurate approach if the operator is able to determine the actual position of the ASIS and GT without ANY soft tissue (i.e., muscle, bursa, subcutaneous tissue) interference. Position of the patient and landmarks The patient is positioned lateral with the side to block up. The dependent leg is extended and the non-dependent leg is flexed at the hip and at the knee and the upper buttock is rotated anteriorly (Sim s position). The ASIS is marked and so is the tip of the GT. Notice that the mark on the skin corresponding to the tip of the GT must represent the posterior projection on the skin of this bony prominence and not its lateral one. The latter would artificially add length to the ASIS-GT line (by taking into account soft tissue) making its midpoint artificially lateral and away from the sciatic nerve. The midpoint of this transverse line is found and from here a perpendicular line is projected caudally and medially for 3 cm. This is the point of needle insertion. Several authors have modified the length of the perpendicular line, blaming it for the difficulty with the technique. The length of this line has been modified to measure anything between 2 to 5 cm. In 1974 Winnie and colleagues published in Anesthesiology Review, vol. 1, pages a modification, which combined with the original Labat s are known collectively as the classic technique. They proposed a second transverse line extending from the sacral hiatus (SH) to the tip of the greater trochanter. The distance between these two transverse lines determines the length of the perpendicular line without need for measuring it. The superior and inferior limits of the perpendicular line roughly represent the length (height) of the sacrum and so, according to the authors, with this technique the distance along the perpendicular line will vary with the height of the patient. This seemingly easy concept has a problem when applied to a clinical case. Because the 92

93 transverse diameter of the pelvis is fairly constant (as discussed earlier) a longer perpendicular line (supposedly from a taller patient) would necessarily end closer to the midline, meaning that a taller patient would have a nerve closer to the midline than a shorter patient. This obviously could not be the case. The fact is that the perpendicular line of Labat was not created to be flexible in length. This combined approach, despite its shortcomings is the most commonly used posterior approach to the sciatic nerve in the gluteal area. Technique Usually the block can be completed with a 4, insulated needle, but sometimes a longer needle needs to be used. The needle is advanced, perpendicular to all planes until a twitch from the sciatic nerve is found. If a twitch is still visible at 0.5 ma a slow injection is started with frequent aspirations. If the nerve is not contacted the technique does not have a clear strategy for reposition of the needle. In fact the nerve could be at any point around a 360-degree radius. Local anesthetic and volume We usually like to use 1.5% mepivacaine plus 1:400,000 epinephrine in a volume of ml to provide 3-4 hrs of anesthesia. Ropivacaine % can be used for longer duration. Complications The literature mentions that the absorption from this site is minimal. However, it is important to remember that the branches of the inferior gluteal vessels at this level are large and multiple. It is important to do gentle and frequent aspirations and to inject slow. Because of the vascularity of the region hematomas can develop. The patient lying supine immediately post block could theoretically help to minimize this problem. Dysesthesias in the sciatic or posterior femoral cutaneous nerve are reported more frequently after this block than in other parts of the body. These usually resolve within 1-2 weeks. 93

94 SCIATIC NERVE BLOCK Franco s approach Indications The same indications than for a classic technique. Point of contact with the nerve This is usually a mid-gluteal technique that approaches the sciatic nerve distal to the piriformis in the proximity of the ischium (about the same site than the classic technique). However because caudal to the piriformis the sciatic nerve runs almost parallel to the midline, this technique can be used at any point between mid-gluteal to subgluteal levels. Main characteristics This is a simple technique that relies on one simple anatomical landmark, the intergluteal sulcus, and avoids the need to palpate any buried anatomical landmarks. It is based on simple but not universally known facts: 1. The trajectory of the sciatic nerve in the gluteal region is for the most part parallel to the midline. 2. The width of the adult pelvis is similar in all adults and surprisingly similar in males and females at any given age. Variation in hip width reflects a hormonedependent, gender-related different pattern of fat deposition. In fact most of the differences in the human bony pelvis are limited to the inner pelvis. Thicker bones in the males compensate for the wider inner pelvis of females to make the average bicrestal diameter (total width) 280 mm in males and 275 mm in females. 3. The sciatic nerve is about 10 cm from the midline (intergluteal sulcus). That is, the nerve is at a fixed distance from the midline. Deposition of fat superficial and lateral to the nerve does not affect its position with respect to the midline. What remains highly variable is the depth at which the nerve is located and the distance from the nerve to the lateral side of the patient. Both of these measurements are related to the amount of adipose tissue in the buttocks. Position of the patient and landmarks This block can be performed in lateral decubitus or prone. We prefer to do it almost 100% of the times in the lateral position because that way is less cumbersome, it is more comfortable for the patient and easier to prepare for. Fig 7-3. The patient lies on lateral decubitus. The point of needle entrance is easily found at 10 cm from the midline at about midgluteal level. (On a patient with permission). 94

95 The patient is placed in the lateral position with both hips and knees slightly flexed. The buttocks form a 90-degree angle with the table. Having the patient at straight angles with the table makes the technique easier because the midline of the patient becomes parallel to the table. The midpoint from top to bottom of the intergluteal sulcus is identified from which a 10-cm linear measurement is made, lateral and away from it. This is the point of needle insertion (see figure 7-3). This point can be moved distally, still at 10 cm from the midline, as far caudal as the subgluteal fold. This could be necessary is the buttock is large and the needle is not long enough. Nerve stimulator technique A small skin wheal of local anesthetic is raised plus 2-3 ml of subcutaneous infiltration in the line of insertion of the needle is also given. A 4, insulated needle is usually sufficient. For this technique we usually set the nerve stimulator current at 1.5 ma (2.0 ma in diabetic patients), with a frequency of 1 Hz and pulse duration of 0.1 msec (100 µsec). In some cases a 6 needle is necessary. The needle is advanced slowly and parallel to the midline until it reaches the gluteus maximus muscle. Usually this is evidenced by a local muscular twitch of the buttock. This twitch is very reassuring, telling the operator that the needle-stimulator unit is functional and most importantly, providing information on sciatic nerve depth. If 8 or more cm of a 10 cm needle are necessary to reach the superficial aspect of the gluteus maximus, most likely the needle will prove to be too short to reach the sciatic nerve. If the gluteus maximus is found at a shallower level then the operator advances the needle through the gluteal muscle until the local twitch disappears. For about 1-2 cm deep to the gluteus maximus no twitch is visible as the needle traverses the connective tissue separating the muscle from the nerve. This silence should be soon followed by a twitch resulting from stimulation of the sciatic nerve. The nerve is rarely more than 2 cm deeper to the gluteus maximus. I believe that any of the possible responses from the sciatic nerve (i.e. eversion, dorsiflexion, inversion and plantar flexion) are adequate, provided that the injection is made with a visible response at 0.5 ma or less. There are few reports in the literature that argue in favor of inversion as the best response and eversion as being a response that would produce a higher rate of incomplete or failed blocks. This is not our experience. If no response from the sciatic nerve is obtained deeper to the gluteus maximus muscle, then a reposition of the needle is necessary. Here is very important to take into account the vector effect, the impact that correcting the insertion angle of the needle would have in the distance that the tip of the needle moves from the original point. According to my own calculations at a theoretical depth of 9 cm, a 10-degree correction moves the needle tip 1.6 cm and a 20-degree correction moves it 3.4 cm. Because the nerve is around 1.5 cm wide it is very easy to overshoot the correction. Some useful tips when trying to pinpoint the sciatic nerve When an adequate twitch is found the nerve stimulator current is lowered until a twitch is still visible at 0.5 ma or less. This is done while maintaining visual contact with the twitch. If the twitch becomes weak before reaching 0.5 ma, the current is not lowered any further and instead the operator slowly moves the needle closer to the nerve. 95

96 Logic says that to get closer to the nerve the operator should move the needle deeper in the original direction that the nerve was found. However it doesn t always work that way. It is not infrequent to find that the response fades even more as the needle is inserted deeper. Instead, slightly withdrawing the needle makes the twitch stronger. This can be explained by a flexible needle drifting away from the nerve or passing along one of the sides of the nerve. Whatever the reason, the needle needs to be slightly repositioned to be more in line with the nerve. Deciding whether to correct lateral or medial depends on what type of response is being elicited. Eversion and dorsiflexion are responses from the common peroneal or lateral side of the nerve, while inversion and plantar flexion are responses from stimulation of the tibial or medial component of the nerve. A small correction is then made accordingly on the opposite direction to the side being stimulated. Than can be accomplished by removing the needle only a couple of cm and then (while still partially buried) bend the outside portion of needle to apply a small correction angle to the tip of it. Bringing it out completely and then reinserting it carries a big chance of overshooting the correction. The saphenous or femoral nerves need to be blocked as needed. Ultrasound technique The nerve is identified in cross section as usual. A curved 5-7 MHz probe can be used to identify the sciatic nerve in obese patients. Local anesthetic and volume We commonly use ml of 1.5% mepivacaine usually with 1:400,000 epinephrine fro a 3-4 hr duration of anesthesia. Ropivacaine can be used if longer duration is necessary. Complications Same as classic approach. Pearls The 10 cm measurement is a linear measure that must disregard the individual patient s buttock contour so it can reflect the distance from the midline to outside the ischium. The orientation of the patient s midline needs to be acknowledged. The easiest way to do it is to place the patient in a true lateral position so the patient s midline becomes parallel to the table. If this position is not possible the operator needs to ascertain the degree of inclination of the midline with respect to the table so the needle still can be advanced parallel to the patient s midline. When the nerve is not found at first attempt it could only be located either lateral or medial to the needle. Because of gravity it is more frequent that the distance has been underestimated, so the first correction should be lateral. When reposition is necessary it is very important to keep in mind the vector effect. At a theoretical distance of 9 cm a 10-degree correction will move the needle app 1.6 cm. A 20-degree correction will move it 3.4 cm. This big jump could easily overshoot the correction. A small 10-degree correction usually is all it takes to localize the nerve. 96

97 SCIATIC NERVE BLOCK, SUBGLUTEAL di Benedetto s approach Indications This is a block more suitable for surgery below the knee because it does not reliably block the posterior femoral cutaneous nerve (back of the thigh). It is also frequently used for continuous catheter techniques. Point of contact with the nerve The nerve is approached at or in the vicinity of the subgluteal fold. Main characteristics There are several descriptions of techniques performed at or around the subgluteal fold. Some authors mention Raj s supine approach to sciatic nerve (Anesthesia & Analgesia 1975) as being the first. In fact this is a sciatic block performed between the ischium and greater trochanter (mid-gluteal level), just a few cm caudal to Labat s classic approach. In this technique the lower extremity to be blocked is elevated and flexed at the hip and knee, stretching the buttock tissues. This supposedly brings the sciatic nerve closer to the skin. It is interesting to note that even though this technique is universally known as Raj s supine approach a completely similar technique was introduced a year earlier (1974) by Winnie and colleagues and published in Anesthesiology Review. The technique introduced by Raj was devised for below-the-knee operations. This fact is frequently forgotten and we will revisit it later. The most common infra or subgluteal technique now seems to be the technique introduced by di Benedetto and colleagues out of Italy in 2001 and published in Anesthesia & Analgesia. Patient position and landmarks This block is performed in the Sim s position as the classic technique. The greater trochanter and the ischium are identified and a line is drawn in between the two. A second line from its midpoint is drawn perpendicularly and caudally for 4 cm to find the needle insertion point. According to the authors at this point the operator should be able to palpate a skin depression, which would represent the groove between the biceps femoris and semitendinosus muscles. This is one more instance where anesthesiologists display their love affair with grooves. In fact cadaver dissections show: 1. The subgluteal fold is about 8 cm caudal to the midpoint between ischium and greater trochanter 2. At the subgluteal fold the three components of the hamstring muscles are practically fused together in one single tendon (no groove). More distally a groove could be found between different components and specifically between biceps and semitendinosus, but it is too subtle to be easily palpable through several layers (skin, subcutaneous tissue and thick fascia lata). 3. The sciatic nerve runs under the biceps femoris and not in a groove between biceps and semitendinosus. In many patients a cleavage plane or groove can be clearly seen in the lateral aspect of the posterior thigh. This corresponds to a plane between the tensor of fascia lata laterally 97

98 and biceps femoris medially. This groove does not represent the trajectory of the sciatic nerve in the thigh (the nerve runs medial to it under the cover of biceps). Technique The authors advice to insert the needle perpendicular to the skin until a twitch from the sciatic nerve is obtained. Local anesthetic and volume The same as indicated for classic approach Complications Common to other approaches to the sciatic nerve. 98

99 SCIATIC NERVE BLOCK, SUBGLUTEAL Franco s approach The subgluteal approach can be easily accomplished simply by measuring 10 cm from the midline at the level of the subgluteal fold with the patient lying in lateral decubitus as shown in fig 7-4. Fig 7-4. The needle insertion point in the subgluteal fold is found the same way than in the mid-gluteal area. (On a patient with permission). The technique is accomplished the same way than mid-gluteal approach advancing the needle parallel to the midline, finding a local twitch from the gluteus maximus muscle before arriving to the level of the sciatic nerve. The current is lowered to around 0.5 ma and a slow injection is started. If the nerve is missed at first pass it could only be located medial or lateral to the needle. A small 10-degree reinsertion angle is applied to the needle first lateral and then if necessary medial. Ultrasound technique The fact that the sciatic nerve is more superficial at the subgluteal level makes it more possible for the ultrasound to visualize it at this level. We should remember that the sciatic nerve at this level is still covered superficially by the gluteus maximus muscle. The reason that the nerve is more superficial than in the gluteal area is less amount of fat. The nerve can be visualized with a linear probe at intermediate or low frequency depending on patient s size. Curved probes and lower frequencies for bigger patients. The patient is prone or in lateral position. The in plane or out of plane techniques can be used. A few facts on subgluteal approach 1. This approach consistently misses the posterior femoral cutaneous nerve, so anesthesia of the back of the thigh is only obtained in about 30% of the cases (my own data). The reason is that the posterior femoral nerve is most of the times already superficial (above the fascia) at the level of the subgluteal fold. 2. It is commonly thought that the inferior border of the gluteus maximus muscle coincides with the subgluteal fold, so people believe that an approach at this level would not pass through gluteus maximus muscle. The fact is that subgluteal fold and inferior border of gluteus maximus are two different things. The subgluteal fold is just a fold of the skin that crosses the inferior border of the gluteus muscle 99