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
www.CookCountyRegional.com
Chicago, IL Fourth Edition 2010
This manual is intended for anesthesiology residents, nurse anesthetists and fellow faculty members of the Department of Anesthesiology and Pain Management, Cook County Hospital of Chicago. The writing in these pages reflects th e author’s own views and understanding of various regional anesthesia issues, as well as his interpretation of the pertinent literature. The author has made every effort to give proper credit to outside sources when applicable. Patients and models appearing in this manual provided their written permission to the author, to have their photographs taken for the purpose of teaching. Their decision was voluntary and did not involve compensation of any kind. The photographs of cadaver material shown in these pages, originate from dissections performed by the author in the Anatomy Laboratory of Rush University Medical Center in Chicago, in compliance with Rush University’s University’s guidelines, as well as State and Federal laws and regulations. Care has been taken to confirm the accuracy of the information presented. However, the author is not responsible for errors or omissions, or for any consequences resulting 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 February 2010. However, recommendations and guidelines change, therefore the reader is urged to check for new indications, warnings and precautions.
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For my residents, who make my coming to work intellectually challenging and pleasurable and to the memory of my father
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CONTENTS Chapter 1: Introduction General considerations……………………… considerations……………………………………………………… ………………………………………….. ………….. 8 Patient selection and premedication……………………………………………………. premedication……………………………………………………. 8 Monitoring………………………………………………… Monitoring…………………… ………………………………………………………..… …………………………..… 9 Outcome issues…………………… issues………………………………………………… ……………………………... ....................................... .................................... 9 Airway and regional anesthesia………………………………………………………….11 anesthesia………………………………………………………….11 References………………………………………………… References……………………… …………………………………………………… ………………………….. ..… …12 Chapter 2: Local Anesthetics Historical perspective………………..…………………………………………………. perspective ………………..…………………………………………………..14 .14 Chemical structure ……………………………… ……………………………………………………………… ……………………………………. ……... .. 15 + channels……………….………………………………....17 Mechanism of action and Na channels……………….……………………………… ....17 Pregnancy and local anesthetics……………………………………………………… anesthetics……………………………………………………….....17 .....17 Fiber size and pattern of blockade………………….…………………………………....17 blockade………………….…………………………………....17 Local anesthetics additives…………….………… additives…………….……………………….………………… …………….……………………… ……..20 ..20 Metabolism………………………….…………………… Metabolism………………… ……….………………………….…………………….. …….……………………......24 ....24 Dibucaine number………………………… number………………………………………………………… ………………………………………...… ………...….. .. 24 Toxicity……………………………………………… Toxicity………………… ………………………………….………………………... …….……………………….........25 ......25 Tumescent anesthesia…………………………… anesthesia…………………………………………………………… ………………………………….. ….........26 .......26 Lipid emulsion……………………… emulsion…………………………………………………… ……………………………………………... ……………….....…...27 Maximum dose……………………… dose…………………………………………………… ………………………………………………… ……………………...29 ...29 Methemoglobinemia……………………………………………………………….....… ..….29 Allergy …………………………… ……………………………………………………… ………………………………………………….. ………………………......30 ....30 References……………………………………………………………………………. References……………………………………………………………………………......34 .....34 Chapter 3: Neuraxial Anesthesia Spinal anesthesia Anatomy………………………………………………………….........................37 Anatomy…………………………………………………………... ......................37 Cerebrospinal fluid………………………… fluid…………………………………………………………... ……………………………….........38 ......38 Site of action and indications…………………………………….........................39 indications…………………………………….........................39 Determinants of spread………………………………… spread……………………………………………………… …………………….. …39 ..…39 Anesthesia duration………………………… duration………………………………………………………… ………………………………........41 ........41 Side effects and complications…………………………………………….. complications……………………………………………..…… …….41 .41 Postdural puncture headache…………………………………………… headache………………………………………………….…. …….….43 43 Transient neurological symptoms…………………………………………… s ymptoms…………………………………………… ......44 Cauda equina syndrome………………… s yndrome………………………………………………… ………………………………… ….........45 Back pain …………………………… …………………………………………………………… …………………………………….…… …….…….45 .45 Spinal in the outpatient……………………………………………………… outpatient……………………………………………………….. …46 ..… Intrathecal adjuncts………………………… adjuncts………………………………………………... ……………………........................46 .....................46
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Epidural Anesthesia Anatomy………………………………………………………….........................47 Anatomy…………………………………………………………... ......................47 Blockade characteristics………………… characteristics…………………………………………... ……………………….........................47 ......................47 Spread of local anesthetics……………………………………….........................47 anesthetics……………………………………….........................47 Type of needles ne edles and catheters………………………… catheters…………………………………………………… …………………………48 48 Test dose……………………………… dose………………………………………………………… …………………………... ........................48 .....................48 Activating an epidural…………………………… epidural………………………………………………………. …………………………........48 .......48 References…………………………………………………………………………. References…………………………………………………………………………......… .....…49 Chapter 4: Regional Anesthesia and Anticoagulation Introduction…………………………………………………………………………. Introduction……………………………………………… …………………………........51 .......51 Strength and grade of recommendations…………………………………………………51 recommendations…………………………………………………51 Venous thromboembolism…………………… thromboembolism……………………………………………… ………………………………………….51 ……………….51 Risk of bleeding…………………………… bleeding……………………………………………………… …………………………………………….53 ………………….53 Thrombolytics………………………………………… Thrombolytics……………… ……………………………………………………… …………………………………54 ……54 Unfractionated heparin…………………………… heparin………………………………………………………… ……………………………………..54 ………..54 Low molecular weight heparin……………………… hep arin………………………………………………… …………………………………..55 ………..55 Oral anticoagulants…………………………… anticoagulants……………………………………………………… …………………………………………56 ………………56 Thrombin inhibitors………………………………………… inhibitors…………………………………………………………………… …………………………...57 ...57 References………………………………………………… References……………………… ……………………………………………………… ……………………………..59 ..59 Chapter 5: Peripheral Nerve Blocks target………………………….....……………………...61 Bringing the needle close to its target………………………….....……………………...61 Nerve stimulation…………………………………………………………………… stimulation …………………………………………………………………… ...… ...…61 Ultrasound……………………………………………… Ultrasound………………… …………………………………………………………… ………………………………..62 ..62 Nerve injury……………………………………………………………………….…... injury……………………………………………………………………….…......65 ...65 Use of epinephrine…………………………… epinephrine………………………………………………………… ………………………………………….6 …………….66 6 paresthesia……………………………………………… ……………………………………………….6 …………………….66 Persistent Persist ent paresthesia…………………… 6 Pre-existing Pre-existing neurological condition………………………… condition……………………………………………………..6 …………………………..67 7 Electrophysiological testing………………… testing………………………………………………… …………………………………………..6 …………..67 7 Tourniquet…………………………………………………… Tourniquet……………………… ……………………………………………………… ………………………….6 .68 8 References………………………………………………… References……………………… ………………………………………………………. …………………………….70 70 Chapter 6: Upper Extremity Blocks Anatomy of the brachial plexus…………………………………………………...…… plexus…………………………………………………...……..73 ..73 Interscalene block……………………………… block……………………………………………………………… …………………………………...…. …...…...79 ..79 Supraclavicular block…………………………… block…………………………………………………………… ……………………………………… ……….86 .86 Infraclavicular block……………………………… block……………………………………………………………… …………………………………... …......96 ...96 Axillary block………………………………………………………………………... Axillary block………………………………………………………………………......104 ...104 References………………………………………………… References……………………… ……………………………………………………… ……………………………112 112
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Chapter 7: Lower Extremity Blocks Anatomy……………………………………………………………………………… Anatomy……………………………………………… ………………………………..115 ..115 Lateral femoral cutaneous nerve block……………………………………………… block………………………………………………...123 ...123 Femoral block………………………………… block………………………………………………………………… …………………………………… ……..….124 Obturator nerve block………………………………… block……………………………………………………………….. ……………………………..... ... 128 Lumbar plexus block…………………………… block…………………………………………………………… …………………………………… ……....133 ....133 Winnie)………………………………………..…...136 …...136 Sciatic nerve block, classic (Labat- Winnie)……………………………………… Sciatic nerve block, Franco’s……………………………………………………. Franco’s…………………………………………………….……..138 ……..138 Sciatic Sciatic subgluteal nerve block, block , di Benedetto’s……………………………………. Benedetto’s…………………………………….…...144 …...144 Sciatic subgluteal nerve block, Franco’s……………………………………………... Franco’s…………………………………………….....146 ..146 Popliteal nerve block, Franco’s…………………………………………………… Franco’s…………………………………………………….…...148 …...148 References………………………………………………………………………….…...154 …...154 Chapter 8: Continuous Nerve Blocks Introduction………………………………………………………………………… Introduction……………………………………………… ……………………………..15 …..156 6 Benefits……………………………………………… Benefits………………… ………………………………………………………… …………………………………15 ……156 6 catheters………………………………………….15 ……………….157 Stimulating versus non-stimulat ing catheters………………………… 7 Catheter-related problems………………………………………………………………15 pr oblems………………………………………………………………157 7 References…………………………………………………… References……………………… ……………………………………………………....15 ………………………....158 8 Chapter 9: Other Blocks …………………………………………………..160 Trans Abdominal Plane (TAP) Block …………………………………………………..160 Refrences…………………………………………………… Refrences……………………… ……………………………………………………… …………………………..162 ..162
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CHAPTER 1 INTRODUCTION
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General considerations
Regional anesthesia is a combination of techniques (i.e., peripheral or neuraxial) that are able to render part of the human body insensate to pain by selectively interrupting nerve transmission without having to alter the patient’s level of consciousness. In this manual I discuss several aspects related to regional anesthesia, according to the techniques most commonly used in the United States, although with special emphasis on the techniques we perform at Cook County Hospital of Chicago. “art”. As such, it is Regional anesthesia has been traditionally considered an “art”. usually practiced by “artists”, “artists” , who use their particular talents to produce results difficult to reproduce by anesthesiologists devoid of artistic talents. I have a great respect and admiration for all the pioneers who introduced and/or helped popularized the various regional anesthesia techniques available to us now. The anesthesiology community owes them a debt of gratitude for they built the foundations of our current practice. However, I st also believe that the practice of regional anesthesia in the 21 century should be more a science than an art, taking advantage of all the various technologies available to us now. Using technology to help our work does not demean our practice; on the contrary, it makes it more rational, reproducible, and potentially easier and safer. The introduction of ultrasound in regional anesthesia is an example of that. The nerve blocks that we perform, and which I describe in these pages, are based on anatomical, physiological, and pharmacological facts. The endpoints chosen are objective. We use local anesthetic solutions in volumes and concentrations considered adequate and safe by clinical experience. Regional anesthesia practiced in this manner, should likely lead to predictable and reproducible results. Regional anesthesia carries the risks and complications associated with the 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). As with any other anesthetic technique, choosing regional anesthesia requires a thorough assessment that involves the patient, the surgeon, the nature of the procedure and its estimated duration, as well as the anesthesiologist’s level of experience 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 large 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. Traditionally it has been considered that an awaken patient would 8|Page
contribute to the safety of the technique by being able to communicate with us (e.g., pain at injection, early subjective symptoms indicating impending systemic toxicity, etc). This is now controversial since there is some evidence that nerves can be penetrated and injection can be performed intraneurally, although extrafascicular, without pain. Improvements in ultrasound technology with better imaging resolution could potentially improve safety. Monitoring
Every nerve block, whether it is performed in a dedicated room, holding area, OR, PACU or office, must be treated as potentially dangerous. Monitoring blood pressure, heart rate and pulse oximetry, as well as the establishment of an 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 and suction capabilities, must always be readily available. A clear strategy to deal with 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, should that become 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. The inability to give a clear answer comes from paucity of evidence in the literature. Most of the outcome studies available to us 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 it existed, and most of them are retrospective. Lack of randomization raises the possibility of technique bias selection (i.e., regional anesthesia may have been preferred in sicker patients obscuring its potential benefits). Other problems have to do with the parameter chosen for comparison. To compare mortality for example, the sample would have to be extremely large in order to find a statistically significant difference, since mortality under any type of 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. The physiological response to the stress of surgery or “surgical stress response” involves release of local and central mediators leading to increased levels of, among others, cathecolamines, cortisol, aldosterone and renin. It is also frequently associated with hypercoagulability, immune response depression and protein wasting. The release of local tissue inflammatory factors like cytokines and interleukins can be partially blocked by non-steroidal anti-inflammatory drugs and peripheral nerve blocks using local 9|Page
anesthetics. The central response, responsible for the release of cathecolamines and cortisol, can only be blocked by neuraxial blocks using local anesthetics. Determination of hormonal markers for stress can be demonstrated after general anesthesia and after certain regional anesthesia techniques. However, its impact on morbidity has not been clearly established. If physiological parameters are measured (e.g., PO2, O2 sat) the values obtained are frequently better (at least in the short term) after regional than general anesthesia. However, the real impact that better postoperative physiological parameters have on morbidity is not clear. Nonetheless, there seems to be some agreement that regional anesthesia improves the outcome of selective surgical procedures in a number of different ways, including decreased rates of DVT, PE and blood loss. Surgeries most associated with improved outcome after regional anesthesia a nesthesia 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. Mortality rates also 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 rates in DVT and PE and may also involve better peripheral circulation and decreased venous stasis. 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 where 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 after regional anesthesia can be demonstrated. 2. Upper and lower extremity surgery, even though the patients receiving regional anesthesia may have a higher degree of satisfaction, better pain control and fewer side effects like nausea and vomiting, especially immediately after surgery. This difference rapidly disappears at 24 h. An interesting meta-analysis on the subject of comparative outcome was published in December 2000 in the British Medical 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 1997. A total of 141 trials
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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 as to 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% 6. There were also reductions in myocardial infarction and renal failure. The authors concluded that neuraxial blocks “reduce postoperative mortality and other serious complications” c omplications”.. It was not clear whether these effects were due “solely to benefits of neuraxial blockade or partly to avoidan ce of general anaesthesia”. Meta-analysis has the advantage of pooling large number of patients making it possible to study infrequent clinical events. However, it also means putting together trials from different institutions, frequently from different countries and cultures. It remains to be seen whether theseencouraging results can be duplicated, and whether they could apply to other regional anesthesia techniques (i.e., peripheral nerve blocks). Other authors, like Christopher Wu from Johns Hopkins, have shown the benefits of regional over general anesthesia, when non-traditional outcomes are measured. These outcome parameters include patient satisfaction (including analgesia, prevention of nausea and vomiting and discharge readiness), ability to undergo physical rehabilitation, and cost. These so-called so- called “soft” parameters are very important in today’s today ’s cost-conscious practice. Airway and regional anesthesia
For some anesthesiologists managing a difficult airway almost always means securing it. This approach negates the benefits that regional anesthesia can provide when judiciously used. Evidence is lacking to support the superiority of neither approach. We believe, that regional anesthesia, with its capacity to produce safe and dense surgical anesthesia with minimal physiological derangements, should be carefully contemplated, on a case by case basis, in all kind of patients, including those with potential difficult airway. This does not mean that the anesthesiologist should not be prepared at all times to manage the airway, and have at his/her immediate disposal all necessary equipment and personnel to do it. It is important to emphasize also, that attempting to secure the airway in all patients is not completely devoid of risks and could lead to severe morbidity in some cases. In our practice we routinely provide regional anesthesia to patients with challenging airways. These patients include the obese, as well as trauma patients wearing halos and cervical collars. These patients are assessed individually. The discussion needs anesthesiologist’s to involve the patient and the surgeon and must take into account the anesthesiologist’s expertise and familiarity with regional anesthesia. If a regional anesthesia option is selected, a backup plan, that can be readily implemented, must be available at all times. 11 | P a g e
References
1. Liu SS, Carpenter RL, Neal JM. Epidural anesthesia and analgesia. Their role in postoperative outcome. Anesthesiology 1995; 82:1474-1506 2. Sharrock NE: Risk-Benefit Comparisons for Regional and General Anesthesia, In: Finucane BT (ed), Complications of Regional Anesthesia. New York, Churchill Livingstone, 1999, pp 31-38 3. Neal JM, McDonald SB. Regional Anesthesia and Analgesia: Outcome and Cost Effectiveness. In: Neal JM, Mulroy MF, Liu SS (eds), Problems in Anesthesia, Philadelphia, Lippincott, Williams & Wilkins, 2000, pp 188-198 4. Neal JM: Regional anesthesia and Outcome. In: Rathmell JP, Neal JM, Viscomi CM (eds), Regional Anesthesia, The Requisites in Anesthesiology, Philadelphia, Elsevier Mosby, 2004, pp 164-170 5. 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: 1493-504 6. Wu CL, Fleisher LA. Outcomes research in regional anesthesia and analgesia, Anesth Analg 2000; 91: 1232-1242 7. Urban MK: Is Regional Anesthesia Superior to General Anesthesia for Hip Surgery?, In: Fleisher LA (ed), Evidence-Based Practice of Anesthesiology. Philadelphia, Saunders, 2004, pp267-269
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CHAPTER 2 LOCAL ANESTHETICS
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LOCAL ANESTHETICS
The cell membrane’s resting potential is negative and close to the 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 and bringing its potential to -20 mV or more. Local anesthetics are compounds that have 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 potentially neurotoxic if injected intraneurally, especially if that injection is intrafascicular. The neuronal damage may be 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, that is a mixture 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, and then it came cocaine. The native Indians of Peru chewed coca leaves and knew about their cerebral-stimulating effects. The leaves of erythroxylon coca were taken to Europe where Niemann in Germany isolated cocaine in 1860. Carl Koller, a contemporary and friend of Sigmund Freud, is credited with the introduction of cocaine as a topical ophthalmic local anesthetic in Austria in 1884. 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 1944. Recognition of cocaine’s cardiovascular side effects, effects, as well as its potential for dependency and abuse, led to a search for better local anesthetic drugs. Cocaine is a good topical local anesthetic that also produces vasoconstriction and for this reason it is still used by some, for topical anesthesia of the nose and other mucous membranes. Cocaine blocks the reuptake of cathecolamines from nerve endings. Total dose should not exceed 100 mg (2.5 mL of a 4% solution), to avoid systemic effects like hypertension, tachycardia and cardiac arrhythmias. Ropivacaine is the only other local anesthetic able to produce some vasoconstriction, and that effect is weak. Highlights on local anesthesia and related issues
1850s Invention of the syringe and hypodermic hollow needle. 1884 Halsted, an American surgeon, blocks the brachial plexus with a solution of cocaine under direct surgical exposure.
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1885 Wood, in the United Kingdom, is credited with the introduction of conduction anesthesia through hypodermic injection. 1897 Epinephrine is isolated by John Abel at Johns Hopkins Medical School. 1897 Braun in Germany relates cocaine toxicity with systemic absorption and advocates the use of epinephrine. 1898 Bier is set to receive the first planned spinal anesthesia from his assistant Hildebrandt. After CSF is obtained, the syringe is found not fit the needle and therefore no injection could be performed. Bier then performs the first spinal anesthesia on Hildebrandt using cocaine. They both experience the first spinal headaches. 1908 Bier introduces the intravenous peripheral nerve block (Bier block) with procaine. 1911 Hirschel performs the first percutaneous axillary block. 1911 Kulenkampff performs the first percutaneous supraclavicular block. 1922 Gaston Labat of France, a disciple of Pauchet, introduces in the US his book “Regional Anesthesia Its Technic and Clinical Application”, Application”, the first manual of regional anesthesia published in America. 1923 Labat establishes the first American Society of Regional Anesthesia. 1953 Daniel Moore, practicing at Virginia Mason Clinic in Seattle, publishes his Block”. influential book “Regional book “Regional Block”. 1975 Alon Winnie, L. Donald Bridenbaugh, Harold Carron, Jordan Katz, and P. Prithvi Raj establish the current American Society of Regional Anesthesia (ASRA) in Chicago. 1976 The first ASRA meeting is held in Phoenix, Arizona. 1976 Regional Anesthesia Journal, volume 1, number 1 is published. 1983 Winnie introduces his book, Plexus Anesthesia, Perivascular Techniques of Brachial Plexus Block. Date of introduction in clinical practice of some local anesthetics:
1905 procaine; 1932 tetracaine; 1947 lidocaine; 1955 chloroprocaine (last ester type 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 molecule is composed of two parts, a benzene ring (lipid soluble, hydrophobic) and an ionizable amine group (water soluble, hydrophilic). These two parts are linked by a chemical chain, which can be either an ester (-CO-) or an amide (-HNC-). This is the basis for the classification of local anesthetics as either esters or amides. Injecting local anesthetics in the proximity of a nerve(s) triggers a sequential set of events, which eventually culminates with the 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 unfortunately do not necessarily lead into the desired nerve(s). This fact emphasizes the importance of injecting in close proximity to the target nerve(s). The 15 | P a g e
local anesthetic solution then diffuses through tissues; each layer acting as a physical barrier. 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 by keeping the drug close to the site of action and away from metabolism. In addition, the local + anesthetic receptor site in Na channels is thought to be hydrophobic, so its affinity for hydrophobic drugs is 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, the case for most local anesthetics. Newborn infants have very low concentration of AAG, only reaching adult values by 10 months of age. age. The elderly and debilitated also frequently have decreased levels of albumin and other plasma proteins. These patient populations could be at increased risk for toxicity. On the other hand, AAG levels increase during stress and for several days after the postoperative period. Higher levels of AAG lead to decreased levels of unbound fraction of local anesthetics and a decreased potential for local anesthetic toxicity. However, changes in protein binding are only clinically important for drugs highly protein-bound, such as bupivacaine, which is 96% bound, and sufentanil and alfentanil, which are both 92% bound (Booker et al, 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 (95%) = ropivacaine (94%)> tetracaine (85%) > mepivacaine (75%) > lidocaine 65%) > procaine (5%) and 2 chloroprocaine (negligible). This suggests that the binding site for the local anesthetic molecule in the sodium channel receptor protein, may share a similar sequence of amino acids with the plasma protein binding site. 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 16 | P a g e
present as a base. The pka generally correlates with the speed of onset of most local anesthetics. The closer the pka is to physiologic pH, the faster the onset. For example, lidocaine with a pka of 7.7 is 25% non-ionized at pH 7.4. Its onset is therefore faster than bupivacaine, whose pka of 8.1 makes it only 15% nonionized at that pH. One important exception is 2-chloroprocaine that, despite its pka of 9.1, has a very rapid onset. This is usually attributed to the relatively high concentrations (3%) used in clinical practice that are possible thanks to its low toxicity. It has also been 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 hydrophilic, charged fraction is the active form on the Na channel. + The Na channel is a protein structure that communicates the extracellular of the nerve with its axoplasm. It consists of four repeating alpha subunits and two beta subunits, beta-1 and beta-2. 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-methylD-aspartate (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. Under adequate stimulation, 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 actions are exerted on the extracellular side of the channel. Frequency-dependent blockade +
Local anesthetics show more affinity for open Na channels. When a nerve is experiencing a high frequency of depolarization, like during spontaneous pain or voluntary muscle contractions, it becomes more sensitive to blockade, because the + chances of interaction, between local anesthetics molecules and Na channels, increase. The concept of frequency-dependent blockade also explains the greater susceptibility to blockade exhibited by small sensory fibers, as they generate long action 17 | P a g e
potential (5 ms) at high frequency. Motor fibers on the other hand generate short action potentials (0.5 ms) at lower frequency making them more difficult to block. Pregnancy and local anesthetics
Increased sensitivity to local anesthetics, demonstrated as faster onset and more profound block, may be present during pregnancy. Alterations in protein binding of bupivacaine, may result in increased concentrations of active unbound drug in the pregnant patient, increasing its potential for toxicity. Placental transfer is also more active for lipid soluble local anesthetics. 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. The ionized fraction cannot cross back to the maternal circulation, originating what is called “ion trapping”. Therefore, 2chloroprocaine, with its very short maternal and fetal half-lives, is 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 within a nerve (mantle versus core) 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, temperature and touch), and small myelinated A delta fibers (mediating pain and cold temperature) are blocked before A alpha, A beta and A gamma fibers (motor, propioception, touch, and pressure). It has been speculated that in large nerve trunks, motor fibers would be usually located in the outer portion (mantle) of the nerve bundle, therefore more “accessible” accessible ” to local anesthetics. This would help explain why motor fibers tend to be blocked before sensory fibers in large mixed nerves. In contrast, the frequency-dependence of local anesthetic action would favor block of small sensory fibers, as they generate long action potentials at high frequency, whereas motor fibers generate short action potentials at lower frequency.
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(Figure from Morgan’s Clinical Anesthesiology, 3 rd edition, 2006, reproduced with permission)
Modulating local anesthetic action pH adjustment +
The ionized fraction of local anesthetics is the active form in the Na channel, although 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 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; 760-64) 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: 369-377) randomized 180 patients to study the effects of alkalinizing lidocaine, mepivacaine and bupivacaine for nerve 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 accepted that adding bicarbonate to local anesthetics, may speed the onset of local anesthetics solutions that have epinephrine added by the manufacturer 19 | P a g e
(vials have a lower pH), while the effect would be negligible when fresh epinephrine is added to a plain solution. 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 rd bupivacaine raises the pH of the solution to 6.4 (from M ulroy’s Regional Anesthesia, Anesthesia, 3 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 inside the cell. 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 mcg of epinephrine should 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 me ans of its α2-agonist α2-agonist actions. Subarachnoid epinephrine also delays voiding and discharge readiness. The prolongation of effect in peripheral nerve blocks can be 30-60%, 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. In general, epinephrine added to spinal anesthesia prolongs the effect of the less lipid soluble agents like lidocaine and mepivacaine (20-30%). The exception to this rule is tetracaine, a highly lipid soluble agent, that gets the largest prolongation of all spinal local anesthetics (up to 60% in lumbar dermatomes). The usual dose of intrathecal epinephrine is 200 mcg, but doses as small as 50 mcg can be sufficient. In the epidural space the usual dose is 5 mcg/mL. Epinephrine, other than intrathecal, 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 mcg) may be associated with arrhythmias or other undesirable cardiac effects. The potential risk for peripheral nerve ischemia, as a result of epinephrine acting on epineural vessels and vaso nervorum has to be balanced against the lower risk of systemic toxicity, the ability to detect intravascular injection and the prolongation of 20 | P a g e
action. According to Neal (Reg Anesth Pain Med 2003;28:124-134) adding 5 mcg/mL (1:200,000 dilution) prolongs the duration of lidocaine for peripheral nerve blocks from 186 min to 264 min. Adding only 2.5 mcg/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 local anesthetic solutions for nerve blocks has become the standard in our practice, in both diabetics and non-diabetics patients. In 2006 Bigeleisen reported in Anesthesiology a study in which he demonstrated intraneural injection by ultrasound in 72 out of 104 nerves studied in the axilla. The local anesthetic used was a combination of bupivacaine plus lidocaine and contained 3 ucg/mL of epinephrine. The author did not find any evidence of nerve injury in up to 6 month follow up. 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 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, pp 25-31) 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 digits is cited in the literature. Lalonde et al published a multicenter study including 3,110 consecutive cases of use of epinephrine in the fingers and hand from 2002-2004. The authors (surgeons) defined “low dose” epinephrine as 1:100,000 and they reported no instance “of digital tissue loss” (J Hand Surg 2005; 30:1061-67). 30:1061 -67). At this time we do not recommend this practice. Dilution/concentration issues
By definition a 1:1,000 dilution means 1 g solute in 1,000 mL of solution. That is the same than to say 1 mg/mL or 1,000 mcg/mL Thus, if 1:1,000 equals 1,000 mcg/mL, then:
1:10,000 equals 100 mcg/mL 1:100,000 equals 10 mcg/mL 1:200,000 equals 5 mcg/mL 1:400,000 equals 2.5 mcg/mL
Opioids
1. 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.
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The hydrophilic opioid morphine can be used in doses of 0.1-0.3 mg spinal and 13 mg epidural. It has a slow onset of 45 min, providing an analgesic action that th lasts 12-24 h. Morphine reaches the brainstem and 4 ventricle slowly. Delayed respiratory depression (8-10 h) is a risk with all neuraxial opioids, but it 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, more pruritus (60-80%, 20% of it severe), and delayed voiding. It is not suitable for outpatients. Short-acting opioids, such as fentanyl and sufentanil, when added to spinal anesthetics can 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 2.5-10 mcg. Fentanyl spinal is used in doses of 10-25 mcg and 25-150 mcg epidural. Onset occurs at 5-15 min, peak effect at 10-20 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 was approved in 2004. It 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, 10-15 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.
2. 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 intra-articular 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 clonidine produces both vasodilation via sympatholysis and vasoconstriction through receptors on smooth muscle. The cause for its anti shivering and diuretic effects are yet to be established. Side effects, including sedation, hypotension and bradycardia, limit alpha-2 agonists use. Small doses of clonidine (50-75 mcg) have shown to significantly prolong analgesia in spinal, epidural, IV regional, and peripheral nerve blocks, both when injected 22 | P a g e
along local anesthetics and when given orally. Injected intrathecally, they also can delay voiding and can produce orthostasis. Side effects do not occur often at clonidine doses below 1.5 mcg/kg or a total dose less than 150 mcg. Iskandar et al in France in 2001, showed that adding 50 mcg of clonidine to selected nerves (median and musculocutaneous) prolonged mepivacaine sensory anesthesia by 50%, compared to placebo, after a mid-humeral block, 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 half-li fe is only 2 h compared to more than 8 h for clonidine. Dexmedetomidine may offer extended analgesia with lesser side effects. This drug is gaining popularity as a sedative both in the ICU and the OR. 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; 90:710-717) studied the effects of different doses of neostigmine added to bupivacaine spinal. They reported that 50 mcg 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 mcg/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. However, the evidence shows 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.
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METABOLISM OF LOCAL ANESTHETICS Ester local anesthetics
They are rapidly hydrolyzed at the ester linkage by plasma pseudocholinesterase, the same enzyme that hydrolyses acetylcholine and succinylcholine. The hydrolysis of 2chloroprocaine is about four times faster than procaine, which in turn is hydrolyzed about four times faster than tetracaine. However, even tetracaine has a metabolic half-life of only 2.5-3.0 min (Tetzlatt JE. In: Ambulatory Anesthesia Perioperative Analgesia. New York, McGraw-Hill, 2005, p 193). 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, although slower than esters. Elimination half-life for lidocaine is 1.5-2 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 primary metabolic pathway for mepivacaine is oxidation to 3-hydroxy and 4hydroxymepivacaine. This pathway is less developed in neonates resulting in slower metabolism of mepivacaine in newborns th an in adults (Raj’s Regional Anesthesia). 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 24 | P a g e
helps to identify those patients. Dibucaine binds strongly to normal plasma pseudocholinesterase inhibiting its action. This inhibition is reported as a number from 1100 representing the percentage of normal enzyme inhibition, the larger the number the larger the proportion of normal enzyme. A number of 80 or higher means that dibucaine is able to inhibit at least 80% of the enzyme and that the patient is a 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). LOCAL ANESTHETIC TOXICITY
The capacity of a local anesthetic to produce systemic toxicity is directly related to plasma level of unbound drug. This plasma level depends on: 1. Total dose 2. Net absorption, which depends on: vasoactivity of the drug, site vascularity and use of a vasoconstrictor 3. Metabolism and elimination of the drug from the circulation Brown et al reported a 1.2 in 10,000 incidence of systemic toxicity after epidural anesthesia and 19 in 10,000 after peripheral nerve blocks. CNS signs of toxicity usually precedes CV manifestations. According to Mather et al, central nervous system (CNS) and cardiovascular (CV) effects are “poorly correlated with arterial drug concentrations ” and better correlated with the “respective regional venous drainage” drainage ”. According to them, 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: 553-66). 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. The absorption of local anesthetics from different sites is from highest to lowest: endotracheal > intercostal > caudal > epidural > plexus blocks > sciatic/femoral > subcutaneous infiltration. Generally the administration of a 100-mg dose of lidocaine in the epidural or caudal space results in approximately a 1 mcg/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 mcg/mL. The same dose injected in the intercostal space produces a 1.5 mcg/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 2chloroprocaine, which has a plasma half-life of about 45- 60 seconds. For amide local anesthetics like lidocaine peak plasma levels after regional anesthesia primarily result from absorption and usually occur within 1 h (please see difference with tumescent anesthesia). Rodriguez et al studied 10 end-stage renal disease patients coming for A-V fistula (Eur J Anaesthesiol 2001; 18: 171-6). The patients received an axillary block with a total of 650 mg of plain mepivacaine. Plasma levels were studied during 150 min. Peak levels 25 | P a g e
of 8.28 mcg/mL (range 3.83-11.21) were obtained (normal 5 mcg/mL) within 60 min and decreased steadily thereafter. Patients did not exhibit signs of toxicity despite these high plasma levels. 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 mcg/mL Tumescent (diluted) anesthesia for liposuction
The use of highly diluted concentrations of lidocaine (0.1% or less) plus epinephrine (usually 1 mg per liter or 1:1,000,000) allows for painless and bloodless liposuction procedures. Lidocaine bounds to tissue proteins in this subdermal drug reservoir from where it is subsequently slowly released into the systemic circulation. Diluted lidocaine, along with epinephrine-induced vasoconstriction, makes systemic uptake so slow as to match the liver maximum lidocaine clearance capacity of 250 mg/h. Therefore, according to de Jong, “the blood level remains below 5 mcg/mL toxic threshold, despite the administration of many times (e.g., 35 mg/kg) the conventional upper dose limit of undiluted full strength lidocaine” (Int J Cosmetic Surg 2002; 4: 3-7). 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. This is the basis for fractionating of the dose and the use of vasoconstrictors. Toxic plasma levels could rarely result from the slow absorption from the injection site. A sequence of symptoms may include numbness of the tongue, lightheadedness, tinnitus, restlessness, tachycardia, convulsions and respiratory arrest. There is no evidence that patients suffering from seizure disorders are at any increased risk for CNS local anesthetic toxicity, including seizures. The site of action for local anesthetic-induced seizures seems to be the amigdala, part of the limbic system, in the base of the brain. 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 The incidence of CV toxicity with local anesthetics is higher in pregnancy due to higher proportion of unbound fraction. CV toxicity is increased under conditions of hypoxia and acidosis. 26 | P a g e
Toxic plasma concentration thresholds
The following are accepted plasma levels of selected local anesthetics, above which systemic effects are expected in humans: Lidocaine 5 mcg/mL; mepivacaine 5 mcg/mL; bupivacaine 1.5 mcg/mL; ropivacaine 4 mcg/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 therefore, cerebral metabolism and oxygen requirements remain increased. In an interesting study by Mayr et al, out of Innsbruck, Austria (Anesth Analg 2004; 98: 1426-3), the authors induced cardiac arrest in 28 pigs by administering 5 mg/kg of 0.5% bupivacaine and stopping ventilation until asystole occurred. CPR was initiated after 1 min of cardiac arrest. After 2 min the 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. This is in line with current ACLS recommendations of using one single dose of 40U of vasopressin IV before using epinephrine. Little information is available regarding the treatment of local anesthetic cardiovascular toxicity in humans. Animal data suggest: 1. Vasopressin 40 U, IV, single dose, one time only followed by, if needed, high doses of epinephrine (1 mg IV every 3-5 minutes) to support heart rate and blood pressure. 2. Atropine may be useful for bradycardia. 3. DC cardioversion is often successful. 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 20-30 mL of saline or dextrose in water. Bupivacaine toxicity and use of lipid emulsion to treat it
Bupivacaine cardiac toxicity was highlighted in an editorial report by Albright in 1979, in which he described several cases of refractory cardiac arrests in association with the use of bupivacaine (Anesthesiology 1979; 51:285-7). In 2003, Weinberg and 27 | P a g e
colleagues from the University of Illinois, published an interesting paper describing the use of a 20% lipid emulsion in combination with cardiac massage to successfully return normal hemodynamics to 9 out of 9 dogs, after asystole brought by a bolus injection of 10 mg/kg of bupivacaine (Reg Anesth Pain Med 2003; 28:198-202). The results of this study led them to recommend treating bupivacaine-associated cardiac arrest with a 20% lipid emulsion IV. The treatment protocol includes a 1 mL/kg bolus of 20% lipid emulsion (such as intralipid), followed by an infusion of 0.25 mL/kg/min for 10 min, and the continuation of 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 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 vasopressin followed by epinephrine, 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 anesthetic-induced cardiac toxicity. 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 a cardiac arrest, presumably linked to bupivacaine after an interscalene block. They described that after 20 min of cardiac compressions and with the patient in asystole, 100 mL of intralipid IV was given resulting in an apparent “immediate” 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, without any apparent neurological sequelae. In an accompanying editorial, Weinberg suggested having 20% lipid emulsion available in all sites where local anesthetics are used. Also in 2006, soon after Rosenblatt’s R osenblatt’s report, Litz et al reported a case of successful use of intralipid after ropivacaine-induced asystole. More recently, in March 2008, McCutchen and Gerancher reported a case of ventricular tachycardia treated with 150 mg of amiodarone, 10 mL of 20% intralipid and a synchronized countershock of 120 J, after which there was a prompt return to normal sinus rhythm. The authors speculate that the use of intralipid might have prevented the patient from going into cardiac arrest. 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 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
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depression. Therefore, propofol is not indicated to treat local anesthetic-induced cardiac toxicity. Maximum dose
Regional anesthesiologists perform peripheral nerve blocks with an amount of local anesthetics that usually exceeds what traditionally have been considered “maximum “maximum recommended doses” doses ”. However the traditional recommendations are based on extrapolation from animal data that do not necessarily apply to clinical practice. According to Rosenberg et al, the common recommendations for maximum doses, as suggested by the literature, literatur e, “are not evidence based” (Reg Anesth Pain Med 2004; 29: “poor approximation 564-575), and according to Milroy have proven to be “poor approximatio n of safety” (Reg Anesth Pain Med 2005; 30: 513-515). 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, 2001, to discuss the subject. Many papers related to that conference have been published. In a review article by Rosenberg et al (just cited) the authors argue that the safe doses instead should be block specific and related to patient’s age (e.g., epidural), organ dysfunction (especially for repeated doses) and whether the patient is pregnant. They suggest also adding epinephrine 2.5 to 5 mcg/mL, when not contraindicated. The fact is that most of the systemic toxicity occurs with unintentional direct intravascular injection (Mather et al, Reg Anesth Pain Med 2005; 30: 553-566). Methemoglobinemia
Normal hemoglobin contains an iron molecule in the reduced or ferrous form (Fe ), the only form suitable for oxygen transport by hemoglobin. When hemoglobin is 3+ oxidized, the iron molecule is converted into the ferric state (Fe ) or methemoglobin. Methemoglobin lacks the electron that is needed to form a bond with oxygen and therefore 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 like 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 2Hb 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 confirmation by blood analysis. Methemoglobinemia is easily treated by the administration of methylene blue (12mg/kg of a 1% solution over 5 min) or less successfully with ascorbic acid (2 mg/kg). 2+
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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 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 2001-02 demonstrated delayed allergy to lidocaine (ASRA News, February 2006). Eutectic mixture of local anesthetics (EMLA)
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. Anesthesia onset takes between 45 to 60 minutes. Its main use is in children. 2 One or 2 grams of EMLA cream are applied per 10 cm of skin and covered with an 2 2 occlusive dressing (maximum application area 2000 cm or 100 cm in children less than 10 kg). 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. Profile summary of selected agents
1. Procaine: Type: ester Pka: 8.9 Protein biding: 5% Characteristics: intermediate onset, low potency, short duration. Very short halflife (20 sec). Other: it provides a short-duration spinal (potential benefit on outpatients).
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2. 2-Chloroprocaine: Type: ester Pka: 9.3 Protein binding: negligible Characteristics: very fast onset, despite high pka (ability to use higher concentrations could be the reason). Short duration (it has 30 minutes 2-segment regression in epidural). Very short half-life (30 sec). Other: The original preparation contained sodium metabisulfite as a preservative. It was associated with serious neurological deficits when a large injection, planned for epidural, ended 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 this side effect may be secondary to action on paraspinal muscles. The present solution is prepared without preservatives, and no back spasms have been reported. 3. Tetracaine: Type: ester Pka: 8.6 Protein binding: 85% Characteristics: slow onset, high potency, long duration. Short plasma half-life (2.5 to 4 min). Other: early experience with this product at high doses resulted in CNS toxicity, giving it a bad reputation, mostly undeserved. We still use it occasionally in our practice, as lyophilized crystals dissolved in liquid mepivacaine for a final concentration of 0.2% tetracaine. It prolongs duration of surgical anesthesia in peripheral nerve blocks to 4-6 h. Tetracaine also is the drug that gets the longest prolongation from adding epinephrine to spinal anesthesia (up to 60% in the lumbar dermatomes). 4. Cocaine: Type: ester Pka: 8.6 Protein binding: ? Characteristics: slow onset, short duration. Elimination half life 60-90 min. Urinary excretion of unchanged cocaine is usually less than 1%, but it can be up to 9% especially in acid urine. At the end of 4 hours, most of the drug is eliminated from the plasma. Cocaine metabolites (benzoylecgonine and ecgonine) may be present in the urine for 24-36 hours, but some metabolites may be identified for up to 144 h after administration (Ellenhom and Barceloux, 1988). Other: 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, arrhythmias and myocardial ischemia. It is used mainly for topical anesthesia of the nose. Doses below 100 mg (2.5 mL) are usually safe.
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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. 5. Benzocaine: Type: ester Pka 3.5 Characteristics: slow onset, short duration and the only LA with a secondary amine structure that limits its ability to pass through membranes (topical use only). Other: Doses higher than 300 mg can induce methemoglobinemia. 6. Lidocaine: Type: amide Pka: 7.8 Protein binding: 65% Characteristics: intermediate onset and duration, elimination half-life 45-60 min. Other: 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 25-40 mg highly reduce the incidence of TNS. 7. Mepivacaine: Type: amide Pka: 7.6 Protein binding: 75% Characteristics: intermediate onset and duration. Elimination half-life is 2-3 h in adults and 8-9 h in neonates. Other: It produces less vasodilation than lidocaine. It has been used in spinal anesthesia. It has lower (but not zero) incidence of TNS. It is the agent we most commonly use for peripheral nerve blocks. A 1.5% of plain solution provides a short onset and dense surgical anesthesia lasting 2-3 h (3-4 h with 1:400,000 epinephrine). Prolonged postoperative analgesia, as with all other LA, is negligible after single-shot blocks. The primary oxidative metabolic pathway for mepivacaine is less developed in neonates resulting in slower metabolism of mepivacaine in newborns than in adults (Raj’s Textbook of Regional Anesthesia). 8. Bupivacaine: Type: amide Pka: 8.1 Protein binding: 95% Characteristics: high potency, slow onset, long duration. Elimination half-life 33.5 h in adults and around 8 h in neonates. 32 | P a g e
Other: lower concentrations (0.25% and less) produce analgesia with increased motor sparing (desirable in outpatients and obstetrics). Commercial bupivacaine is a 50:50 racemic mixture of the R and S enantiomers. Cardiac arrest associated with bupivacaine is difficult to treat possibly due to its high protein binding and high lipid solubility (please see toxicity). 9. Ropivacaine: Type: amide Pka: 8.2 Protein binding: 94% Characteristics: onset and duration similar to bupivacaine, with slight lesser potency. 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. The S enantiomer is associated with less cardiac toxicity, intermediate between that of lidocaine and bupivacaine. Other: It is a weak vasoconstrictor (only one other than cocaine). At lower concentrations (less than 0.5%) it may show a greater selectivity for sensory than motor blockade than bupivacaine. 10. Levobupivacaine: Type: amide Pka: 8.1 Protein binding: 97% Characteristics: S enantiomer of bupivacaine, very similar to ropivacaine. Not available at this time in the US.
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References
1. Lou L, Sabar R, Kaye A: Local Anesthetics, In: Raj P (ed), Textbook of Regional Anesthesia. New York, Churchill Livingstone, 2002, pp 177-213 2. Brown DL, Fink R: The History of Neural Blockade and Pain Management, In: rd Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, Lippincott-Raven, 1998, pp 3-32 3. Strichartz GR: Neural Physiology and Local Anesthetic Action, In: Cousins MJ, rd Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, LippincottRaven, 1998, pp 35-54 4. Tucker GT, Mather LE: Properties, Absorpton, and Disposition of Local rd Anesthetic Agents, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, Lippincott-Raven, 1998, pp 55-95 5. Covino BG, Wildsmith JAW: Clinical Pharmacology of Local Anesthetic Agents, rd In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, Lippincott-Raven, 1998, pp 97-128 th 6. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4 edition. New York, McGraw-Hill, 2006, pp 263-288 rd 7. Mulroy MF: Regional Anesthesia, 3 edition. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 1-63 8. Liu SS, Joseph RS: Local Anesthetics, In: Barash PG, Cullen BF, Stoelting RK (eds), Clinical Anesthesia. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 453-471 9. DiFazio CA, Carron H, Grosslight KR, et al. Comparison of ph-adjusted lidocaine solutions for epidural anesthesia. Anesth Analg 1986; 65: 760-64 10. Hilgier M. Alkalinization of bupivacaine for brachial plexus block. Reg Anesth 1985;10: 59-61 11. Booker PD, Taylor C, Saba G. Perioperative Peri operative changes in α1-acid α1-acid glycoprotein concentrations in infants undergoing major surgery. Br J Anaesth 1996; 76: 365368 rd 12. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice, 3 edition. Philadelphia, Lippincott-Raven, 1999, pp158-181 13. Tetzlaff JE: Local anesthetics and adjuvants for ambulatory anesthesia. In: Steele SM, Nielsen KC, Klein SM (eds), Ambulatory Anesthesia Perioperative Analgesia. New York, McGraw-Hill, 2005, pp 193-205 14. Weinberg GL et al. Lipid emulsion infusion rescues dogs from bupivacaineinduced cardiac toxicity. Reg Anesth Pain Med 2003; 28:198-202 15. Mayr VD, Raedler C, Wenzel V, et al. A comparison of epinephrine and vasopressin in a porcine model of cardiac arrest after rapid intravenous injection of bupivacaine. Anesth Analg 2004; 98:1426-3 16. 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; 28:124-134 17. Rosenberg PH, Veering VT, Urmey WF. Maximum recommended doses of local anesthetics: A multifactorial concept. Reg Anesth Pain Med 2004; 29: 564-575.
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18. Mulroy MF. MF. Local anesthetics: Helpful science, but don’t forget the basic clinical steps (editorial). Reg Anesth Pain Med 2005; 30: 513-515. 19. Mather LE, Copeland SE, Ladd LA. Acute toxicity of local anesthetics: Underlying pharmacokinetic and pharmacodynamic concepts (A review article). Reg Anesth Pain Med 2005; 30: 553-566 20. Horlocker TT. 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): 543-4 21. Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics: Incidence and preventative measures (editorial). Reg Anesth Pain Med 2002; 27(6): 556-61 22. Horlocker TT, Wedel DJ. Local, anesthetic toxicity-Does product labeling reflect actual risk? Reg Anesth Pain Med 2002; 27(6): 562-567 23. Weinberg GL. Current concepts in resuscitation of patients with local anesthetic cardiac toxicity. Reg Anesth Pain Med 2002; 27(6): 568-575 24. Myer Leonard. Carl Koller: Mankind’s greatest benefactor? The story of local anesthesia. J Dent Res 1998; 77:535-8 25. De Jong R. Tumescent anesthesia: lidocaine dosing dichotomy. Int J Cosmetic Surg 2002; 4: 3-7 26. Nordstrom H, Stange K. Plasma lidocaine levels and risks after liposuction with tumescent anaesthesia. Acta Anaesthesiol Scand 2005; 49: 1487-1490 27. Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006; 105:217-8 28. Litz RJ, Popp M, Stehr SN, et al. Succesful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion. Anaesthesia 2006; 61: 800-801 29. Rodriguez J, Quintela O, Lopez-Rivadulla M, 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: 171-176 30. Kamibayashi T, Maze M. Clinical uses of 2-adrenergic agonists. Anesthesiology 2000; 93:1345-9 31. Tanoubi I, Vialles N, Cuvillon P, et al. Systemic toxicity with mepivacaine following axillary block in a patient with terminal kidney failure. Ann Fr Anesth Reanim 2006; 25:33-5 32. McCutchen T, Gerancher JC. Early Intralipid Therapy May Have Prevented Bupivacaine-Associated Cardiac Arrest. Reg Anesth Pain Med 2008; 33: 178-180 33. Bigeleisen PE. Nerve puncture and apparent intraneural injection during ultrasound-guided axillary block does not invariably result in neurological injury. Anesthesiology 2006; 105: 779-783
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CHAPTER 3 NEURAXIAL ANESTHESIA
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SPINAL ANESTHESIA
It is one of the easiest and most reliable techniques of regional anesthesia. The very small doses of local anesthetics used to produce spinal anesthesia are devoid of 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 failed attempt, by his assistant Hildebrandt, to perform a spinal anesthesia on him, and his successful spinal on Hildebrandt. Both of them became the first patients suffering from 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 cranially at the foramen magnum, as a continuation of the medulla oblongata. It terminates caudally 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 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 ventral (motor) and dorsal (sensory) horns. The white matter is described as having anterior, lateral and posterior white columns. There are 31 pairs of spinal nerves; each one being formed by two roots, a ventral or motor root and a dorsal or sensory root. The dorsal root has the dorsal root ganglion. Because the spinal cord of an adult is shorter than 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 dural 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 th nerve exits through the occipital bone and C1, the 8 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 the local anesthetic solution, as we will review later. 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 37 | P a g e
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. 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, and typically enters the spinal canal through a single intervertebral foramen between T8 and L3. This important branch is at risk of damage during retroperitoneal dissections (e.g., surgery on the distal aorta), which could lead to ischemia of the spinal cord. A case of transient paraplegia after neurolytic celiac plexus block on a pancreatic cancer patient was reported in 1995 by Wong and Brown. The proposed mechanism was reversible arterial spasm post injection of ethanol solution. Planes between the surface of the skin and subarachnoid space
The needle used to perform a diagnostic spinal tap or a spinal anesthesia needs to cross the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, duramater and arachnoid, before reaching the subarachnoid space and CSF. 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 from there 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 0.3-0.4 mL/min. The CSF volume in the brain is between 100-150 mL. The volume of CSF below T12, where most of the spinal anesthetics are performed is, according to Hogan and collaborators, widely variable among individuals, ranging from 28-80 mL. CSF volume is decreased with increased abdominal pressure, like the one accompanying pregnancy and obesity. Therefore, increased abdominal pressure could potentially lead to higher spread of a neuraxial blockade. Composition of cerebrospinal fluid and serum in humans
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 2O)
CSF 141 2.9 2.5 2.4 124 21 61 28 7.31 289
Serum 140 4.6 5.0 1.7 101 23 92 7000 7.41 289 38 | P a g e
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 1.0003. 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 local anesthetic 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 of hypobaric solutions 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 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 and subsequently they become the limits for spread. Determinants of local anesthetics spread in the spinal fluid 1. Major factors Baricity acting together with gravity Position of patient (except isobaric solutions) Dosage, rather than volume or concentration
Baricity is the main factor that determines local anesthetic spread in the subarachnoid space. It obviously works in conjunction with gravity and patient position. When plain local anesthetics are used, total dose is more important than injected volume or concentration. Van Zundert et al reported in 1996, that a 70 mg dose of plain subarachnoid lidocaine produced the same quality of spinal block over a wide range of concentrations and volumes. Sheskey et al in 1983 demonstrated similar sensory levels with 10 mg of plain bupivacaine, at different concentrations and volumes. However, doses of 15-20 mg of plain bupivacaine produced higher sensory levels of spinal (T2-T4 39 | P a g e
level) than 10 mg (T5-T8 level). When hyperbaric bupivacaine or tetracaine solutions are used, similar levels of spinal blocks are obtained at different doses, when the concentration is maintained constant. In the case of hyperbaric bupivacaine, it seems that this applies as long as the dose is higher than 7.5 mg. Above this dose the level is determined by baricity acting along with the curvatures of the spine, patient position, and gravity. In general, the higher the spread the shorter the duration of the sensory blockade, because the concentration of the drug decreases from the point of injection. 2. 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. 3. No effect Addition of vasoconstrictors Barbotage (aspirating and injecting technique to produce CSF turbulence) Age Gender Techniques Sitting, midline approach Sitting position is commonly used for neuraxial blocks. It may be the preferred position in patients whose midline may be difficult to determine, like obese patients. The position of the iliac crest is frequently used to determine the L4-L5 interspace. However, accumulation of adipose tissue around the patient mid section, could lead to a higherthan-desired level for needle placement. The Closed Claims Project shows cases of spinal cord injury by the spinal needle, in which the level of needle placement was grossly underestimated. I suggest instead using the upper end of the intergluteal sulcus to determine the position of the sacral hiatus. In adults the L5-S1 interspace is around 10 cm (4 inches) cephalad to this point (height of the sacrum). This measurement in adults should always be distal to the termination of the spinal cord at L1. 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 y appreciable “saddle” or “lateralized” 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 40 | P a g e
Paramedian approach
In some elderly patients, 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. 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 dependent on vascular absorption and does not involve metabolism of local anesthetics 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 seen side effect. It is mainly the result of venous pooling with decreased cardiac output secondary 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 after spinal anesthesia the decrease in systemic vascular resistance is less than 15%. This is because arterioles retain intrinsic tone and do not dilate maximally. The magnitude of the blood pressure decrease depends on the extent of sympathetic blockade, intravascular volume, and cardiovascular status. Preloading the patient with 250-500 mL, while frequently used, is unsupported by the evidence. A mild vasopressor like ephedrine in 5-10 mg increments and fluid are all that is usually necessary to treat hypotension. Ephedrine is usually the drug of choice because it produces vasoconstriction and increases cardiac output. Phenylephrine is a good second choice especially if tachycardia is present. It causes vasoconstriction, and it could decrease the cardiac output. Trendelenburg position can alleviate the venous pooling, but may produce an even higher spinal level. Elevating the legs with the patient sitting at 30-45 degrees is a good compromise.
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2. Bradycardia When the sympathetic block reaches T2 level, the cardioacelerator fibers are blocked and the vagus action is unopposed. The extent to which heart 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 30-45 minutes of spinal. The Bezold-Jarisch reflex has been implicated. This reflex would be triggered by 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, ventilator support, use of vasopressors, and atropine and fluid replacement as needed. Miscellaneous physiologic effects
1. Respiratory Arterial gases are usually unaffected in patients 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. 42 | P a g e
4. Endocrine and metabolic Spinal anesthesia, but not general anesthesia, blocks the hormonal and metabolic stress 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. 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. The pain characteristics, involving exacerbation in the upright position and relief in the recumbent position, remain the main 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. They found that dural fibers are arranged in laminas with fibers in all 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 may stimulate more inflammation than a cleaner cut does. The inflammatory response and edema would then limit the leakage of CSF. This observation agrees with the surprisingly low incidence of PDPH after continuous spinal anesthesia with an 18-gauge epidural needle and 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 is accompanied by a decreased risk of PDPH.
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In the issue of PDPH:
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%. Continuous spinal with 20 gauge catheters is not likely to produce PDPH in an older patient population. Obstetric patients undergoing spinal anesthesia with small pencil point needles show a 3-4% rate of post dural puncture headache. Conservative treatment involves bed rest, IV or oral fluids, acetaminophen and NSAIDs. Hydration and caffeine stimulates production of CSF. Epidural blood patch with 15-20 mL of autologous blood, injected at the same original puncture level or one space below, is a 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 12- 24 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, cauda equine syndrome. 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:
A higher (but variable) incidence after lidocaine spinal. Decreasing the concentration of lidocaine to 0.5% does not appear to change this incidence. 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 (e.g., higher doses/concentration of local anesthetics and the addition of vasoconstrictors), do not have an effect on TNS.
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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 that it is very rarely associated with 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 at this point. However do not use it for ambulatory surgery in lithotomy position or knee arthroscopy (high risk). On the other hand, the incidence of TNS after inguinal hernia with lidocaine spinal is only 8%, after C-section is 0-8% and after 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 have 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.
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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 performed on these patients without apparent problems. The risk has to be evaluated on an individual basis. Spinal anesthesia in the outpatient setting
A few years ago spinal anesthesia was favored for same day surgery patients. However, widely available, poorly-soluble general anesthetic agents and LMA have decreased its use. Home readiness involves short duration and in many institutions, 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 concentrate 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. Procaine and very small doses of bupivacaine plus narcotics have been used in the outpatient setting with variable success. 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. Ben-David et al in 1997 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 doses below 25 mcg. 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). 46 | P a g e
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 it is 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 12-24 mL of local anesthetic 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.
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Techniques Lumbar epidural It is 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 should be safer. An accidental dural puncture (“wet tap”) could result in spinal cord damage at higher levels. Thoracic epidural It is technically more challenging and has a greater risk for spinal cord injury. It is rarely used as the primary anesthetic. Many people prefer the paramedian approach in the thoracic level, because of the extreme obliquity of the thoracic spinous processes. Epidural needles The Tuohy needle is the most commonly used. A typical needle is 17-18 gauge, 3.5 inches long. It has a blunt bevel with a gentle curve of 15-30° at the tip. The blunt tip it, after the ligamentum flavum has been pierced. helps push the dura away, “tenting” it, Epidural catheters They provide the means for continuous infusion. Usually they are 19-20 gauge in size. The needle bevel is directed in the desired direction (not a guarantee for catheter final location) and the catheter is advanced 2-6 cm. A short insertion increases the chance for accidental dislodgement. The farther in, 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 important because of the large doses of LA injected into the epidural space. The classic test dose is 3 mL of 1.5% lidocaine (45 mg) with 1:200,000 of epinephrine (15 mcg). The 45 mg of lidocaine, if intrathecal, should produce spinal anesthesia. The 15 mcg of epinephrine, if intravascular, should produce at least a 20% increase in heart rate th within 30 sec or 30 beats between 20- 40 sec (Barash’s, 5 edition, 2006). In patients who are beta blocked the heart rate increase may not happen and an increase in systolic th pressure of 20 mmHg or more may be more reliable ( Barash’s 5 edition, 2006). The use of epinephrine as a test dose in obstetrics is controversial. Some suggest instead the use of only 30 mg of lidocaine or 5 mg of bupivacaine. 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 50-70 minutes, for lidocaine is 90-150 minutes and for bupivacaine is 200-260 minutes.
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References th
1. Snell R: Clinical Anatomy for Medical Students, 5 edition. Boston, Little, Brown and Company, 1995 2. Bernards CM: Epidural and Spinal Anesthesia, In: Barash PJ, Cullen BF, th Stoelting RK, Clinical Anesthesia, 5 edition. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 691-717 rd 3. Mulroy MF: Regional Anesthesia, 3 edition. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 65-118 4. Wong G, Brown D. Transient paraplegia following alcohol celiac plexus block. Reg Anesth 1995; 20: 352-355 5. Hogan QH. Magnetic resonance imaging of cerebrospinal fluid volume and the influence of body habitus and abdominal pressure. Anesthesiology 1996; 84; 1341-1349 6. Bridenbaugh PO, Greene NM, Brull SJ, Spinal (Subarachnoid) Neural rd Blockade, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, Lippincott-Raven, 1998, pp 203-241 7. Cousins MJ, Veering BT: Epidural Neural Blockade, In: Cousins MJ, rd Bridenbaugh PO (eds), Neural Blockade, 3 edition. Philadelphia, LippincottRaven, 1998, pp 243-320 8. Salinas FV: Pharmacology of Drugs Used for Spinal and Epidural Anesthesia and Analgesia, In: Wong CA (ed), Spinal and Epidural Anesthesia. New York, McGraw-Hill, 2007, pp 75-109 9. Sheskey MC, Rocco AG, Bizzarri-Schmid M, et al. A dose-response study of bupivacaine for spinal anesthesia. Anesth Analg 1983; 62: 931-935 10. Van Zundert AAJ, Grouls RJE, Korsten HHM, et al. Spinal anesthesia: Volume or concentration-What matters? Reg Anesth 1996; 21: 112-118 11. Giroux CL, Wescott DJ. Stature estimation based on dimensions of the bony pelvis and proximal femur. J Forensic Sci, 2008; 53: 65-68 12. Reina MA, de Leon-Casasola OA, Lopez A, 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: 393-402 13. Swisher JL. Spinal Anesthesia: Past and Present. In Problems in Anesthesia, 2000:12; 141-147 14. Ben-David B, Solomon E, Levin H, et al. Intrathecal fentanyl with small-dose dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth Analg 1997: 85; 560-565 15. Pollock JE. Transient neurological symptoms: etiology, risk factors, and management. Reg Anesth Pain Med 2002:27; 581-86 th 16. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4 edition. New York, McGraw-Hill, 2006, pp 289-323
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CHAPTER 4 REGIONAL ANESTHESIA AND ANTICOAGULATION
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Regional anesthesia in the patient receiving antithrombotic an tithrombotic or thrombolytic therapy
The American Society of Regional Anesthesia (ASRA) convened its Third Consensus Conference on Regional Anesthesia and Anticoagulation. The new guidelines were published in the January-February 2010 issue of the ASRA Journal. This chapter is mainly based on these guidelines. Epidural hematoma is defined as a rare, but potentially catastrophic complication of spinal or epidural anesthesia. The introduction of low molecular weight heparin (LMWH) in the United States coincided with an increased number of reported cases of epidural hematoma. Although, it can happen spontaneously, its incidence increases with age, associated abnormalities of the spinal cord or vertebral column, underlying coagulopathy, difficult needle placement and an indwelling catheter in the presence of anticoagulation. The actual incidence of hemorrhagic complications in association with neuraxial anesthesia is unknown, but has been estimated at less than 1 in 150,000 for epidural and less than 1 in 220,000 for spinal anesthesia. Recent studies suggest that this incidence may be higher, some say as high as 1 in 3,000 in selected populations. At the moment there is no laboratory model to study this problem and its rarity precludes a prospective randomized study. As a result the ASRA consensus represents the opinions of experts based on case reports, clinical series, pharmacology, hematology and risks factors for surgical bleeding. Strength and grade of recommendations A cornerstone in evidence-based medicine is the quality of the available evidence. The validity of the recommendation improves with the quality of the evidence. There are three levels of strength of recommendation according to the quality of the available evidence: A: Highest level of evidence. These are randomized clinical trials and meta analysis. Because neuraxial bleeding is rare this type of evidence is mostly not available. B: Inconsistent or limited quality patient-oriented evidence. These are observational and epidemiological series. Depending on the quality of these studies and the degree of risk reductions showed, recommendation from these sources may be categorized as level of evidence A or B. C: recommendations derived from case reports or expert opinion.
The recommendations are also graded to indicate the strength of the guideline and the degree of consensus: Grade 1: represents general agreement on the efficacy. Grade 2: Notes conflicting evidence or opinion. Grade 3: Suggests that the procedure may not be useful and possibly harmful (e.g., epidural procedure in a patient receiving twice-daily LMWH). Venous thromboembolism VTE This is an important health care problem. Neuraxial anesthesia has been associated with improved patient outcomes, including mortality and major morbidity. This probably results from the “attenuation of the hypercoagulable response” and
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decreased venous thrombosis after these techniques. However the beneficial effect of neuraxial techniques on coagulation is insufficient as the sole method of thromboprophylaxis. As a result, anticoagulants, antiplatelets and thrombolytic medications are commonly used in the prevention and treatment of thromboembolism. Nearly all hospitalized patients have at least one risk factor and 40% of patients have 3 or more risk factors (according to Geerts et al, as cited by the 2010 ASRA statement). The following is a table for risk factors for VTE taken from the 2010 ASRA statement:
Accordingly, most hospitalized patients benefit from some type of thromboprophylaxis. The following table, also taken from the ASRA 2010 statement, lists the recommended prophylaxis according to risk:
Because of concerns with surgical bleeding associated with thromboprophylaxis, the American Academy of Orthopaedic Surgeons (AAOS) published its own guidelines 52 | P a g e
in 2007 for the prevention of symptomatic PE in patients undergoing total joint replacement. The following table taken from the 2010 ASRA guidelines shows the AAOS recommendations:
Administration of thromboprophylaxis In terms of agents and doses, the 2010 ASRA statement recommends to follow the American College of Chest Physicians ACCP guidelines advising the clinicians to follow the manufacturer-suggested dosing guidelines (Evidence Grade 1C). Risk of bleeding Bleeding, especially intracranial, intraspinal, intraocular, mediastinal or retroperitoneal, is the most feared complication of anticoagulant and thrombolytic therapy. Risks factors include increased age, female sex, history of gastrointestinal bleeding, concomitant aspirin use and length of therapy. During warfarin therapy an INR of 2.0 to 3.0 is associated with a 3% low risk of bleeding during a 3-month treatment period. Stronger regimens (INR >4) increase the risk of bleeding significantly to 7%. The incidence of hemorrhagic complications during therapeutic anticoagulation with IV or subcutaneous heparin is less than 3% and even lower with LMWH. Thrombolytic therapy is associated with the highest risk of bleeding, with major bleeding occurring in 6% to 30% of patients treated with thrombolytic therapy for DVT, ischemic stroke, or ST elevation myocardial infarction. There is no significant difference in the risk of bleeding among thrombolytic agents. The addition of potent anticoagulants (LMWH, hirudin) or antiplatelets (glycoprotein IIb/IIIa agents) therapy increases even more the risk of major bleeding. “Therefore, although thromboembolism remains a source of significant perioperative morbidity and mortality, its prevention and treatment are also associated with risk” (2010 ASRA statement, page 67).
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Anesthetic management of the patient receiving thrombolytic therapy These patients are at risk of serious bleeding. We will discuss several situations: 1. Patients scheduled to receive thrombolytic therapy: Avoid performing lumbar punctures and neuraxial anesthesia and avoid thrombolytic therapy for 10 days if these procedures have been performed (evidence Grade 1A). 2. Patients who have received thrombolytic therapy: Do not perform spinal or epidural procedures (Evidence Grade 1A). Data not available as to how long we need to wait. 3. Patients who have received neuraxial blocks at or near the time of fibrinolytic and thrombolytic therapy: Neurological monitoring every 2 hours or less “for an appropriate interval”. If epidural catheter present avoid drugs producing sensory and motor block to facilitate neurological assessment (Evidence Grade 1C). 4. Patient with an epidural catheter who unexpectedly received thrombolytic therapy: There is no definite recommendation as to when to remove it. They suggest to measure fibrinogen levels (one of the last clotting factors to recover) for appropriate timing of catheter removal (Evidence Grade 2C). Anesthetic management of the patient receiving unfractionated heparin (UFH) There is a long experience in the management of these patients. However recent guidelines suggesting a three-time dose (thrice daily) of subcutaneous heparin for some patients and its potential for increased bleeding have prompted a modification to the ASRA guidelines as follows:
concomitant use of 1. Daily review of patient’s medical records to identify the concomitant other drugs affecting coagulation like antiplatelets, LMWH and oral anticoagulants (Grade 1B). 2. Patients receiving 5000 U of UFH twice daily do not have contraindication for neuraxial techniques. The risk of bleeding may be reduced by delay of the heparin dose until after the block. The risk may be increased in debilitated patients after prolonged therapy (Grade 1C). 3. The safety of neuraxial blocks on patients receiving more than twice daily dose or doses greater than 10000 U of UFH daily has not been established. Suggest frequent neurological exam if neuraxial has been done (Grade 2C). 4. Patients receiving heparin for more than 4 days (heparin-induced thrombocytopenia) should have a platelet count before neuraxial block and catheter removal. 5. Combining neuraxial techniques with intraoperative anticoagulation with heparin during vascular surgery is acceptable with the following recommendations (Grade 1A): a. Avoid the technique in patients with other coagulopathies. b. Delay heparin administration for 1 hr after needle placement. c. Remove catheter 2-4 hr after the last heparin dose; re-heparin 1 hr after catheter removal.
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d. Monitor the patient postoperatively to provide early detection of motor blockade. Avoid local anesthetics through catheter. e. The occurrence of bloody or difficult neuraxial technique may increase risk, but data does not support mandatory cancellation. Risk-benefit discussion with surgeon about proceeding. f. Insufficient data exist about risk of bleeding when neuraxial techniques are combined with the full anticoagulation of cardiac surgery. They suggest neurological monitoring and avoidance of local anesthetics (Grade 2C). Anesthetic management of the patient receiving LMWH The extensive European experience is useful to us. The 2010 ASRA consensus respects the labeled dosing regimens of LMWH as established by the Food and Drug Administration. Although it is impossible to eliminate the risk of neuraxial hematoma previous recommendations have been deemed useful.
1. The anti-Xa level is not predictive of the risk of bleeding. Recommend against the routine use of it (Grade 1A). 2. Antiplatelets and other anticoagulants administered in conjunction with LMWH increase the risk of spinal hematoma. Avoid concomitant use of antiplatelets drugs, unfractionated heparin, or dextran regardless of LMWH dosing regimen (Grade 1A). 3. The presence of blood during neuraxial technique does not necessitate postponement of surgery. Recommendation to delay initiation of LMWH for 24 hr in discussion with the surgeon (Grade 2C). 4. Preoperative use of LMWH: a. Patients receiving LMWH can be assumed to have altered coagulation. Recommend needle placement at least 12 hr after the LMWH last dose (Grade 1C). b. Patients receiving higher doses of LMWH, such as enoxaparin 1 mg/kg every 12 hrs, enoxaparin 1.5 mg/kg daily, dalteparin 120 U/kg every 12 hrs, dalteparin 200 U/kg daily, or tinzaparin 175 U/kg daily, the recommendation is to delay neuraxial technique for at least 24 hrs (Grade 1C). c. Patients given a dose of LMWH 2 hrs preoperatively (general surgery patients) the recommendation is to avoid neuraxial techniques because of peak anticoagulant activity (Grade 1A). 5. Postoperative use of LMWH: Patients to undergo postoperative LMWH prophylaxis may safely undergo single-injection and continuous catheter techniques. Management is based on total daily dose, timing of the first postoperative dose and dosing schedule (Grade 1C): a. Twice-daily dosing. This dosing is associated with increased risk of spinal hematoma. The first dose of LMWH should be administered no earlier than 24 hrs postoperatively. Indwelling catheters may be left in 55 | P a g e
place overnight but must be removed before initiation of LMWH, and the first dose should be delayed for 2 hrs after catheter removal. b. Single-daily dosing. The first postoperative LMWH dose should be administered 6-8 hrs postoperatively and the second no sooner than 24 hrs later. Indwelling catheters may be safely maintained although it should be removed a minimum of 10-12 hrs after the last dose of LMWH. Subsequent dosing should not be given for at least 2 hrs after catheter removal. No other drugs with effect in coagulation should be given because of risk of additive effects. Regional anesthetic management of the patient on oral anticoagulants The management of patients receiving perioperative warfarin controversial.
remains
1. In the first 1-3 days after warfarin discontinuation the coagulation status (reflected primarily by factors II and X levels) may not be adequate despite a decrease in the INR (indicating a return of factor VII activity). Adequate levels of II, VII, IX and X may not be present until the INR is normal. The recommendation is that warfarin must be stopped 4-5 days prior to the procedure and the INR measured before a neuraxial block is attempted (Grade 1B). 2. Avoid using other drugs with anticoagulation effect like aspirin and other NSAIDs, ticlopidine, and clopidogrel, UFH, and LMWH (Grade 1A). 3. In patients who are likely to have an enhanced response to the drug, it is recommended to use the available algorithms to guide in the dosing based on desired indication, patient factors, and surgical factors (Grade 1B). 4. In patients receiving an initial dose of warfarin before surgery, the recommendation is to check the INR prior to neuraxial block if the first dose of warfarin was administered more than 24 hrs earlier or if a second dose has been administered (Grade 2C). 5. In patients receiving low-dose warfarin therapy during epidural analgesia, the suggestion is to monitor the INR daily (Grade 2C). 6. For patients on warfarin therapy receiving epidural analgesia neurologic testing of motor and sensory function should be performed routinely. To facilitate the neurologic evaluation keep the local anesthetics to a minimum (Grade 1C). 7. As warfarin therapy is initiated it is suggested that neuraxial catheters should be removed with an INR of less than 1.5. This value correlates hemostasis with clotting factor activity levels greater than 40%. The suggestion is to keep neurologic testing after catheter removal for at least 24 hrs (Grade 2C). 8. In patients with INR more than 1.5 but less than 3 the suggestion is to remove catheters with caution after reviewing medication records for other medications affecting coagulation that may not affect the INR (e.g., NSAIDs, clopidogrel, ticlopidine, UFH, LMWH (Grade 2C). It is also recommended to check neurological status before catheter removal and continued until the INR has stabilized at the desired prophylaxis level (Grade 1C). 56 | P a g e
9. In patients with INR greater than 3 and an indwelling catheter, the recommendation to hold or reduce the warfarin dose (Grade 1A). No definitive recommendation can be made for removal of catheters in patients with therapeutic levels of anticoagulation (Grade 2C). Anesthetic management of the patient receiving antiplatelet an tiplatelet medications Antiplatelet medications exert diverse effects on platelet function. These drugs include NSAIDs, thienopyridine derivatives (ticlopidine and clopidogrel) and platelet glycoprotein (GP) IIb/IIIa antagonists (abciximab, eptifibatide, tirofiban). There is no wholly accepted test, including the bleeding time, to guide antiplatelet therapy.
1. NSAIDs seem to present no added significant risk of spinal bleeding related to neuraxial techniques. No specific concerns exist at this time about this drugs and the timing of single-shot or catheter insertion or removal (Grade 1A). 2. In patients receiving NSAIDs, the recommendation is not to perform neuraxial techniques if other drugs like oral anticoagulants, UFH, and LMWH are being used concurrently. Cyclooxygenase-2 (cox-2) inhibitors have minimal effect on platelet function and should be considered in patients requiring antiinflammatory therapy in the presence of anticoagulation (Grade 2C). 3. The actual risk of spinal hematoma with ticlopidine and clopidogrel and the GP IIb/IIIa antagonists is unknown. Recommendations are based on labeling precautions and the clinical experience (Grade 1C). a. On the basis of labeling and surgical experience the waiting period between discontinuation of a drug and neuraxial block is: i. ticlopidine: 14 days ii. clopidogrel: 7 days. If a neuraxial block is indicated between 57 days after its discontinuation, normalization of platelet function should be documented. b. Platelet GP IIb/IIIa inhibitors have a profound effect on platelet aggregation. Neuraxial techniques should be avoided until platelet function has recovered. This time is: i. Abciximab: 24-48 hrs ii. Eptifibatide and tirofiban: 4-8 hrs. Anesthetic management of the patient receiving herbal therapy Herbal drugs by themselves do not interfere with the performance of neuraxial techniques. The recommendation is against mandatory discontinuation of herbs or avoidance of regional techniques in these patients (Grade 1C). Anesthetic management of patients receiving thrombin inhibitors (desirudin, lepirudin, bivalirudin, and argatroban) In these patients the recommendation is not to perform neuraxial techniques (Grade 2C).
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Anesthetic management of the patient receiving fondaparinux The actual risk is unknown. Until further experience is available, performance of neuraxial techniques should be avoided. Anesthetic management of the anticoagulated parturient In the absence of large series of neuraxial technique in pregnant women receiving anticoagulation the recommendation is to follow the ASRA guidelines for the rest of surgical patients (Grade 2C). Anesthetic management of the patient undergoing plexus or peripheral block The recommendation is to apply the ASRA guidelines for neuraxial techniques (Grade 1C).
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References
1. Neal JM: Neural Blockade and Anticoagulation. In: Regional Anesthesia, The Requisites in Anesthesiology. Rathmell J, Neal J, Viscomi C (eds). Philadelphia, Elsevier Mosby, 2004, pp 151-156 2. Bergqvist D, Wu CL, Neal JM. Anticoagulation and Neuraxial Regional Anesthesia: Perspectives. [Editorial] Reg Anesth Pain Med 2003; 28: 163-166 3. Horlocker tt, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: Defining the risks (The Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 2003; 28: 172-197 4. Horlocker TT, Wedel DJ, Rowlingson JC, Enneking FK, Kopp SL, Benzon HT, Brown DL, Heit JA, Mulroy MF, Rosenquist RW, Tryba M, Yuan CS. Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy. American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med 2010; 35: 64-101
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CHAPTER 5 PERIPHERAL NERVE BLOCKS
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Peripheral Nerve Blocks
A successful peripheral nerve block results from injecting an adequate volume of an adequate concentration of local anesthetic in the proximity of the target nerve(s). Intraneural injection (especially intrafascicular) might be harmful to the nerve and can lead to permanent damage. Therefore, a balance must be achieved between the need to get close to a nerve 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 a 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 pulse of the femoral artery can be used to locate the femoral nerve located lateral to it, and the pulse of the axillary artery can guide the injection of the terminal branches of the brachial plexus in the axilla. This anatomical method is extremely operator-dependant with good success in the hands of the few and limited success in the hands of the majority. This method does not take into account anatomical variations, lacks depth perception and can not gauge proximity to a nerve with any degree of certainty. Therefore, the needle might end up too far from the nerve (failed block) or too close to it (intraneural). 2. Paresthesia: this technique requires 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, as referred by the patient, helps the practitioner locate the position of the needle. At this time the needle is withdrawn a few mm, before the injection is started, to decrease the risk of intraneural injection. anesthesia”, was For the longest time, Moore’s dictum “no paresthesia no anesthesia”, the “law of the land” in regional anesthesia. Works by Selander and others, starting in the 1970s, have questioned the safety of this practice. Although, there is not enough evidence to believe that paresthesias lead to nerve damage, there seems to be enough circumstantial evidence to be cautious, especially if repeated paresthesias are elicited. 3. Nerve stimulation: the idea of locating mixed nerves by electrical stimulation was developed in Germany in 1912 by Perthes. However, it was not until 1962 when Greenblatt and Denson introduced a portable, transistorized nerve stimulator that was suitable for the clinical setting. 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 61 | P a g e
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). A visible response at lower currents (less than 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, capable of eliciting a visible response, is a reliable indicator of critical proximity. 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. 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 microsec). 4. Ultrasound: It is the latest and most sophisticated piece of technology introduced to the practice of regional anesthesia and has already caused a revolution. It is the only method that can provide real time assessment of the position of the needle with respect to the nerve, as well as an image of the surrounding structures. An added advantage is that the practitioner is able to see the spread of the local anesthetic, giving him/her the chance to more accurately predict the success of the technique as well as the need for supplementation. Ultrasound could theoretically produce warming of tissues or gas formation. This technology is still expensive, and requires competency on interpretation of cross-section anatomy from “grainy” images. However, it has been rapidly progressing and in many centers, including ours, is the main method used to perform regional blocks of every kind. Characteristics of ultrasound
The human ear can hear sounds between 20 and 20,000 Hz (cycles per second) or 20 KHz. Ultrasounds waves travel at a higher frequency than the highest frequency detectable by the human ear. Ultrasound waves used in medicine usually are in the 1 to 20 MHz range (1 MHz = 1 million Hz). 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. This transition plane is seen as a hyperechoic line on the screen. The ultrasound is delivered from a small probe that contains piezoelectric crystals that under the influence of an electric current are made to vibrate producing a wave of ultrasonic sound. The ultrasound waves in the form of a narrow beam travel through tissues at a speed that depends on the nature of the human tissues, but for calculations and image production is assumed to be an average value of 1,540 m/sec. This value closely approximates the speed of ultrasound through soft tissue (1,540 m/sec), muscle (1,580 m/sec), blood (1,560 62 | P a g e
m/sec), but differs to the speed through bone (4,000 m/sec), lung (500 m/sec) or air (330 m/sec). Part of the ultrasound waves are reflected back to the transducer, especially at tissue interfaces, where the mechanical energy is converted back to electrical energy. The information is then processed by the software of the ultrasound machine to generate an image. Therefore, the transducer delivers ultrasound for part of the time and for part of the time it “listens” listens” for the returned waves. The distance is calculated as a function of the time it takes for the waves to return. Tissues with high density like bone reflect most of the waves and produce a bright image, known as hyperechoic. A tissue like blood that permits easy passage of the ultrasound waves through it appears dark or anechoic. The rest of tissues present intermediate characteristics between anechoic o hypoechoic to hyperechoic. Better images are obtained when the probe is perpendicular to the structure being searched (e.g., nerve, needle). This is because more bouncing sound waves can be detected by the transducer. Changes as small as 10 degrees from the perpendicular can distort the echogenicity of a nerve, reducing the amount of waves returning to the transducer and decreasing the quality of the image. This is known as anisotropy, the change of the quality of the echo image as a result of change in the angle of incidence of the probe with respect to the target structure. Tendons characteristically have higher anisotropy than peripheral nerves. Short versus long axis views
The most common way to identify a peripheral nerve is through a transverse scan of it, it , also called “short axis view”. This provides a cross section image of the nerve(s) and surrounding structures. A “long axis view” view ” of a nerve is also possible, although sometimes more challenging, because the nerves trajectories are not necessarily linear. In addition, in a long axis view the operator looses the ability to readily recognize lateral and medial sides of the nerve on the 2-dimensional image obtained. In plane versus out of plane techniques
of plane” with respect to The needle can be advanced “in plane” or “out of plane” the main axis of the probe. In the in plane approach the needle is advanced in coincidence with the long axis of the probe, in the same plane of the ultrasound beam. This makes possible the visualization of the needle as it advances toward the target nerve(s). Good needle visualization depends on its angle of insertion, with the best visualization obtained when the needle trajectory is parallel to the probe. As the angle of penetration increases (deeper targets) the difficult to visualize the needle also increases. When the insertion angle is more than 45 degrees with respect to the plane of the probe the needle cannot be visualized anymore. At this point tissue movement and injection of small amounts of local anesthetics can help determine the location of the needle tip. 63 | P a g e
With the out of plane approach the needle is advanced perpendicular to the main axis of the probe, so only the tip of the needle can be visualized at the point where it crosses under the ultrasound beam. The tip is seen as a very hyperechoic bright point on the screen. The main advantage of an out of plane technique, from my perspective, is that the trajectory of the needle to the target is shorter. Regardless of the approach the goal is to bring the tip of the needle into the proximity of the nerve(s) for injection. High versus low frequency probes
High frequency probes (8-15 MHz) are usually linear probes that provide good resolution, but limited penetration (3-4 cm). These probes are used at different levels of the brachial plexus, abdominal wall and at different locations in the lower extremity. For deeper structures, lower frequency (4-7 MHz) curved probes are needed providing a wider field and deeper penetration at the expense of resolution. Deep scanning of intra abdominal organs requires frequencies of 35 MHz The quality of the image is also affected by other factors like compound imaging (the capture of different views of structures before producing an image) and color Doppler. We will refer again to ultrasound when we describe individual techniques. Insulated versus non insulated needles
Insulated needles are the needles most commonly used in conjunction with nerve stimulation and ultrasound techniques nowadays in the United States, Europe and other parts of the world. The current applied to this needle concentrates at its tip, 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. Short versus long-bevel needles
Standard needles have a tip 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 needles, the damage was less frequent as the fibers were pushed away by the advancing needle. This concept has been challenged by Rice et al. According to these authors it may be more difficult to penetrate a nerve fascicle with a short-bevel needle than with a sharp needle, but should it occur, the lesions may be more severe. Recently in 2009 Sala64 | P a g e
Blanch and collaborators published in Regional Anesthesia and Pain Medicine a study in which sharp long beveled versus blunt short beveled (30 degrees) needles were introduced into a sciatic nerve of a human cadaver. After the punctures the specimen was investigated under the microscope for evidence of fascicular damage. They demonstrated that with either needle was very difficult to penetrate the fascicles. In fact they found no histological evidence of fascicular damage with short beveled needles and only 3.2% of fascicular damage (4 fascicles) with sharp needles. Nerve injury
Persistent paresthesias can occur after regional anesthesia, although severe neurologic injury is extremely rare. Neal estimates the incidence of persistent neuropathy after regional anesthesia to be less than 0.4%. A large survey by Auroy et al in France in 1997, involving 71,053 neuraxial blocks and 21,278 peripheral nerve blocks, showed a low incidence (0.03%) of nerve complications after regional anesthesia. The survey showed that neurological deficits although low, were relatively more frequent after spinal (70%) than either epidural (18%) or peripheral nerve block (12%). In two thirds of the cases of neuropathy after spinal, and 100% of the cases after epidural, a paresthesia was elicited either by the needle or during the injection. Among the neurological deficits that developed after non-traumatic spinals, 75% of them were in association with the use of 5% hyperbaric lidocaine. Cheney et al in 1999 reviewed the American Society of Anesthesiologist closedclaims database and found that out of 4,183 claims, 670 (16%) were considered “anesthesia-related “anesthesia-related nerve injury” injury ”. Injury to the ulnar nerve represented 28% of the total, and in 85% of the cases it was associated to general anesthesia. Other nerve injuries were brachial plexus in 20%, lumbosacral trunk in 16% and spinal cord 13% and these were more related to regional anesthesia. In 31% of the brachial plexus injuries the patient had experienced a paresthesia with the needle or during injection. They concluded that prevention strategies are difficult because the mechanism for nerve injury, especially of the ulnar nerve, is not apparent. Lee et al in 2004 conducted a new review of the Closed Claims Data for the 1980 to 1999 period focusing in regional anesthesia. A total of 1,005 regional anesthesiarelated claims were reviewed. These claims were 37% obstetric related and 63% nonobstetric. All regional anesthesia, obstetric claims were related to neuraxial anesthesia/analgesia. In 21% of the non-obstetric claims, peripheral nerve blocks were involved. The most common block was axillary block (44%). Upper extremity blocks were more involved in claims than lower extremity blocks. Nerve injury temporary or permanent was claimed in 59% of the peripheral nerve injury claims. Death or brain damage was usually the result of cardiac arrest associated with neuraxial block. Pneumothorax accounted for 10% of the claims and “emotional distress” was claimed in 2% of the cases. Eye blocks accounted for 5% of the claims. Regional anesthesia could result in nerve damage directly from a needle or catheter or be the result of ischemia or other unknown mechanism. Ischemia could be the potential result of vasoconstrictor use or by an intraneural injection that produces an increase of the intraneural pressure leading to nerve ischemia. Local anesthetic toxicity could play a role in cauda equina syndrome and transient neurological symptoms. 65 | P a g e
Another mechanism of nerve injury could be hematoma and infection leading to scar formation. It has been a common belief in regional anesthesia that nerve puncture and intraneural injection lead to nerve damage. In 2006 Bigeleisen published in Anesthesiology a study that seems to discredit this notion. In his study conducted under ultrasound guidance 21 of 26 patients had nerve punctures of at least one nerve, and 72 out of 104 nerves had intraneural injection (2-3 mL). A 6 month follow up failed to demonstrate nerve injury. Incidentally it is important to notice that the local anesthetic mixture injected (bupivacaine plus lidocaine) contained 3 microgr/mL of epinephrine. Since peripheral nerves are formed by neural tissue (fascicles) and connective tissue, it is possible to penetrate the nerve (intraneural), but still be extrafascicular. In 2004 Sala-Blanch et al reported in Anesthesiology two cases of inadvertent intraneural, extrafascicular injection after anterior approach of the sciatic nerve block with nerve stimulation performed in two diabetic patients, as evidenced by CT scan. These two cases also demonstrate that painless nerve punctures and even intraneural (although extrafascicular) injections are possible without apparent sequelae. A preexisting neurological injury should always be documented. It is important to realize that nerve damage can occur perioperatively for a reason other than regional anesthesia. Nerves can be injured during surgery by direct trauma, use of retractors and tourniquets and by improper positioning. Nerves can also be damaged postoperatively by a tight cast or splint, wound hematoma or surgical edema. Use of epinephrine
Epinephrine-containing local anesthetic solutions may theoretically produce nerve ischemia by vasoconstriction of the epineural and perineural blood vessels. Patients at increased risk would be those with previous impaired microcirculation (e.g., diabetics). There is no evidence at this time to suggest a detrimental effect of epinephrine in regional anesthesia, as used in clinical practice. Epinephrine has been used extensively and presumably safely in regional anesthesia. As mentioned earlier in reference to nerve injury, in 2006 Bigeleisen reported intraneural injection in the axilla with local anesthetic without apparent problems. It is interesting to mention that the author injected local anesthetic containing 3 microgr/mL of epinephrine. We use epinephrine 1:400,000 (2.5 microgr/mL) extensively, in all kind of patients, and we appreciate its role as indicator of inadvertent intravascular injection (please see further discussion on epinephrine in local anesthetic chapter). Persistent paresthesia, Clinical presentation
The symptoms can appear within 24 h after the injury, but sometimes they do not present until days or weeks after the offending procedure took place. The degree of symptoms is usually related to the severity of the injury. The cases are usually mild with symptoms like tingling and numbness that usually disappear within weeks, or more rarely they can progress to severe cases of neuropathic pain and motor involvement that can last months and even years.
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Pre-existing neurologic condition and regional anesthesia an esthesia
A pre existing neurologic condition per se is not a contraindication to regional anesthesia. However a careful preoperative assessment must be performed, and any neurological deficit must be documented in the patient’s chart. A thorough discussion with the patient and the surgeon is always important. Certain progressive neurologic conditions like multiple sclerosis, acute poliomyelitis, amyotrophic lateral sclerosis and Guillian Barre syndrome are relative contraindications to regional anesthesia, because the development of new symptoms postoperatively may be confused with complications from the nerve block. In these cases the risks and benefits must be carefully evaluated before proceeding with regional anesthesia. In 2006 Koff et al published in Anesthesiology a case of severe plexopathy after an ultrasound-guided interscalene block in a patient with multiple sclerosis. 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, provided that all preexisting neurological deficits are well documented in the chart. Persistent paresthesia prevention and management
In order to minimize the risk of neurologic injury after regional anesthesia the anesthesiologist needs to consider several factors, including procedure, patient and surgeon. A meticulous nerve block technique, avoiding direct trauma to the nerve and appropriate selection of local anesthetic volume and concentration are important. The role of vasoconstrictors, especially low dose (1:400,000), on clinical development of neural ischemia, has not been elucidated. When a neuropathy develops in the postoperative period, a prompt evaluation is necessary and a multidisciplinary approach, with participation of neurology, radiology, and surgery, is recommended. A detailed history must be obtained including the timing and nature of symptoms. A physical exam should look for any signs of hematoma or infection. A neurological exam by a neurologist is also crucial. Electrophysiological testing
Although electrophysiological studies remain normal for 14 to 21 days after the injury, ordering them early could help establish a baseline and rule out any preexisting condition. These tests have limitations, as they only assess large motor and sensory fibers and not small unmyelinated fibers. They usually include nerve conduction velocity studies and electromyography and sometimes may include evoked potentials. 1. Sensory Nerve Conduction Studies They assess functional integrity of sensory nerves by measuring amplitude and velocity of peripheral nerve conduction. Injuries involving fascicular damage primarily show a decrease in the amplitude of the action potential, a sign that the impulses are being transmitted by a reduced amount of fibers. Conduction velocity in these cases may be minimally affected. When the lesion is
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demyelinating, like the ones seen after tourniquet compression, nerve conduction velocity is greatly affected while the amplitude remains normal. 2. Electromyography It records electrical activity in the muscles helping to locate the denervated muscles in reference to the level at which the nerve damage has occurred. Within 2-3 weeks post injury, spontaneous activity can be recorded from the muscle, in the form of sharp waves and muscle fibrillation. After 3 months the pattern may injuries, change, as nerve regeneration by “sprouting” takes place. In permanent injuries, electromyography remains abnormal. Use of tourniquet Use of crude compression devices to control surgical bleeding from the extremities, can be, according to Bailey, traced back to ancient Rome. The term “tourniquet” was apparently first used by Petit in France in 1718 to describe a mechanical screw-like contraption that he introduced to provide surgical hemostasis. Lister in 1864 was the first surgeon who used a tourniquet to produce a bloodless surgical field. Modern tourniquet devices have a microprocessor, use an air pump and are able to accurately and safely maintain the desired pressure. A fail-safe mechanism protects from pressure ever exceeding 500 mmHg. Tourniquet time: Recommended tourniquet time varies, but the most commonly accepted limit is 2 hours. This recommendation is based on a work by Wilgis, published in 1971 in which he demonstrated more acidosis after 2 hours of ischemia. Surgeons should be made aware when the 2-hour limit has been reached and the tourniquet should be deflated at that time, unless the procedure is at a crucial time. This communication with the surgical team needs to be documented in the chart. Despite the widely accepted 2-hour limit, Klenerman, as cited by Bailey, showed minimal muscle damage with tourniquet times not exceeding 3 hours, using electron microscopy. Some people advocate deflating the tourniquet at 1.5 h for 5-15 minutes followed by an additional 1.5 h of inflation time. Tourniquet inflation pressure: It is believed that inflation pressure is more important of a factor than time in influencing injury. It is recommended to use the minimum inflation pressure that accomplishes ischemia. In general 100 mmHg above the systolic pressure is a common setting. Roekel and Thurston in 1985 showed that 200 mm Hg for the upper extremity and 250 mm Hg for the lower extremity were adequate parameters. Adding layers of padding is important. Wrinkles in the padding should be avoided, since they may become pressure points. Tourniquet associated problems: The exsanguination with an Esmarch bandage prior to tourniquet inflation causes an increase in preload, which can be significant when bilateral tourniquets are used in the lower extremities. Eliminating circulation in part of one extremity also can lead to an increase in afterload. This may cause problems in patients with cardiac problems and decreased cardiac output. Exsanguination of lower extremities has also been associated with pulmonary embolism and cardiovascular collapse.
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Some patients may develop post-tourniquet nerve palsy, affecting more frequently larger motor fibers than sensory fibers. These lesions are usually reversible. The magnitude and duration of the compression dictate the severity of the injury. Patients can also develop “post-tourniquet syndrome”, a clinical picture characterized by interstitial edema, arm weakness and numbness secondary to cell injury and alteration or permeability. It usually resolves within a week. When the tourniquet is deflated blood pressure drops (sudden drop in preload and afterload) and heart rate increases as blood rushes into an ischemic, vasodilated bed (reactive hyperemia). Carbon dioxide and potassium levels increase and so does lactic acid leading to acidosis. These effects peak at about 3 minutes post deflation. Ther e is also a decreased in patient’s temperature. Tourniquet pain: It is commonly observed despite signs of otherwise good anesthesia of the extremity. Unpremedicated volunteers refer intolerable pain by 30 minutes. Signs of tourniquet pain, manifested as a gradual rise in blood pressure, are also observed under neuraxial blocks and general anesthesia. Patients report this pain under the tourniquet and distal to it. Controversy exists as to how this pain is transmitted. De Jong and Cullen in 1963 proposed that tourniquet pain was transmitted by small non-myelinated sympathetic fibers. However tourniquet pain can arise even when high thoracic levels of anesthesia are present. It seems that tourniquet pain is transmitted, as other painful sensations, by A-delta myelinated fibers and C unmyelinated fibers. Tourniquet pain is usually described as burning, cramping or heaviness. The burning and aching sensations, characteristics of ischemia, are believed to be conducted by unmyelinated fibers (MacIver and Tanelian, 1992), while the sharp pain, usually a small component of tourniquet pain, is transmitted by A-delta fibers. MacIver and Tanelian proposed that C fiber activation by ischemia-induced alterations are responsible for tourniquet pain. They studied in an in-vitro model the effects of ischemic alterations (i.e., hypoxia, hypoglycemia, lactic acid, and decreased ph) on Adelta and C pain fibers. They showed that hypoxia and hypoglycemia induced under ischemia, increased C fiber tonic action potential activity, but did not affect A-delta fibers. Increased lactate and decreased pH did not alter the discharge frequency of C fibers in this model. The activation of C fibers by ischemia products seems crucial in tourniquet pain. Whether these C fibers eventually enter the spinal cord at a level above the somatic nerve block is debatable.
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References
1. Mulroy MF: Complications of Regional Anesthesia, In: Mulroy MF, Regional rd Anesthesia, 3 edition. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 29-41 2. Selander D, Dhuner KG, Lundborg G. Peripheral nerve injury due to injection needles used for regional anesthesia. Acta Anaesth Scan 1977; 21: 182-188 3. Rice ASC, McMahon SB. Peripheral nerve injury caused by injection needles used in regional anaesthesia: Influence of bevel configuration, studied in a rat model. Br J Anaesth 1992; 69: 433-438 4. Selander D: Peripheral Nerve Injury After Regional Anesthesia, In: Finucane BT (ed), Complications of Regional Anesthesia. New York, Churchill Livingstone, 1999, pp 105-115 5. Horlocker TT: Persistent paresthesia, In: Atlee JL (ed), Complications in Anesthesia. Philadelphia, W.B. Saunders Company, 1999, pp 290-292 6. Auroy Y, Narchi P, Messiah A, et al. Serious complications related to regional anesthesia. Results of a prospective survey in France. Anesthesiology 1997; 87: 479-486 7. Cheney FW, Domino KB, Caplan RA, et al. Nerve injury associated with anesthesia: A closed claims analysis. Anesthesiology, 1999; 90: 1062-1069 8. Lee LA, Posner KL, Domino KB, et al. Injuries associated with regional anesthesia in the 1980s and 1990s: A closed claims analysis. Anesthesiology, 2004; 101: 143-152 th 9. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4 edition. New York, McGraw-Hill, 2006, pp324-358 pp324-358 10. Hebl JR: Peripheral Nerve Injury, In: Neal JM, Rathmell JP, Complications In Regional Anesthesia and Pain Management. Philadelphia, Saunders Elsevier, 2007, pp 125-140 11. Hadzic A: Textbook of Regional Anesthesia and Acute Pain Management. McgRaw-Hill, 2007 12. Sites BD: Introduction to Ultrasound-Guided Regional Anesthesia: Seeing Is Believing, In: Schwartz AJ (ed), ASA Refresher Courses in Anesthesiology, 2006, pp 151-163 13. Bailey MK: Use of the Tourniquet in Orthopedic Surgery, In: Conroy JM, Dorman H (eds), Anesthesia for Orthopedic Surgery. New York, Raven Press, Ltd, 1994, pp 79-88 14. MacIver MB, Tanelian DL. Activation of C fibers by metabolic perturbations associated with tourniquet ischemia. Anesthesiology 1992; 76: 617-623 15. Hamid B, Zuccherelli L: Nerve Injuries, In: Boezaart AP (ed), Anesthesia and Orthopedic Surgery. New York, McGraw-Hill, 2006, pp 405-419 16. Darmanis S, Papanikolaou A, Pavlakis D. Fatal intra-operative pulmonary embolism following application of an Esmarch bandage. Injury 2002; 33: 761-764 17. Lu CW, Chen YS, Wang MJ. Massive pulmonary embolism after application of an Esmarch bandage. Anesth Analg 2004; 98: 1187-1189
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18. Martin G, Breslin D, Stevens T: Anesthesia for Orthopedic Surgery, In: Longnecker DE, Brown DL, Newman MF, Zapol WM (eds), Anesthesiology. New York, McGraw Hill, 2008, pp 1541-1557 19. Bigeleisen PE. Nerve puncture and apparent intraneural injection during ultrasound-guided axillary block does not invariably result in neurological injury. Anesthesiology 2006; 105: 779-783 20. Sala_Blanch X, Pomes J, Matute P, Valls-Sole J, Carrera A, Tomas X GarciaDiez A. Intraneural injection during anterior approach for sciatic nerve block. Anesthesiology 2004; 101: 1027-1030 21. Koff MD, Cohen JA, McIntyre JJ, Carr CF, Sites BD. Severe brachial plexopathy after an ultrasound-guided single-injection nerve block for total shoulder arthroplasty in a patient with multiple sclerosis. Anesthesiology 2008; 108: 325328 22. Sala-Blanch X, Ribalta T, Rivas E, Carrera A, Gaspa A, Reina MA, Hadzic A. Structural injury to the human sciatic nerve after intraneural needle insertion. Reg Anesth Pain Med 2009; 34: 201-205
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CHAPTER 6 UPPER EXTREMITY NERVE BLOCKS
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UPPER EXTREMITY BLOCKS Anatomy of the brachial plexus Roots
The brachial plexus is most frequently formed by five roots originating from the ventral divisions of spinal nerves C5 through T1. After exiting through the corresponding intervertebral foramen, the roots of the plexus are found in the cervical paravertebral space, between the anterior and middle scalene muscles. In the cervical region the spinal roots emerge above the corresponding cervical vertebrae, as seen in figure 6-1. Because there are 8 cervical nerves but only 7 cervical vertebrae, starting with T1 the spinal roots emerge below the corresponding vertebra (e.g., T1 exits between T1 and T2).
Fig 6-1. Left supraclavicular area. The sternocleidomastoid, scalene muscles, great vessels, soft tissue and fascias have been removed. The vertebral artery is shown in red. The roots of the plexus are seen exiting in between two vertebrae. The dome of the pleura is shown in blue at the bottom of the image. (Dissection by Dr. Franco. Copyrighted image).
The distance from C5 to T1 roots is large and irreducible, and equal to the height of four vertebrae. This fact in itself could help explain the frequent lack of dense anesthesia in the C8-T1 dermatomes after an injection performed at the level of the C5C6 roots (interscalene block). Another important and frequently ignored reason is the expansive wave created by the pulse of the subclavian artery and felt mostly by the distal roots of the plexus (C8-T1), the lower trunk and its divisions. Because the local anesthetic diffuses to points of least resistance, this expanding pulsatile force may keep the local anesthetic from reaching the most distal elements of the plexus. In addition to knowing the formation of the plexus and its architecture throughout its trajectory, it is also important from my perspective to understand the plexus in terms of its relative surface area at different locations. The five roots occupy an area that is elongated in the frontal plane, but very narrow in the sagittal plane (anteroposterior). When the five roots combine together to form three trunks, not only there is a 40% 73 | P a g e
reduction in the number of nerve structures (from 5 to 3), but also the trunks become physically contiguous, as shown in figure 6-2, helping reduce their combined surface area. In fact this is the point at which the brachial plexus is reduced to its smallest surface area. This striking convergence of innervation is unique to the brachial plexus and has no parallel in the lower extremity and helps explain the rapid onset and high success rate of the supraclavicular approach. The surface area of the plexus increases again when the trunks originate six divisions although they stay together so the small increase in surface area is compensated by a larger surface of absorption. The surface area increases the most at the level of the axilla where the plexus gives off the terminal branches.
Fig. 6-2. Left supraclavicular area. The SCM, great vessels and fascias have been removed. The trunks (S, M, I) of the plexus are seen emerging in between the anterior scalene (AS) and medial scalene (MS). Also shown are the anterior (a) and posterior (p) divisions of the upper trunk and its supraescapular branch (supr), the subclavian artery (SA) and vertebral artery (VA). (Dissection by Dr. Franco. Copyrighted image).
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 superior aspect 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 superior aspect of the first rib, behind the subclavian groove.
Brachial plexus structure: 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 (app 1cm) 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, which is innervated by the intercostobrachial nerve, a branch of the 74 | P a g e
second intercostal nerve. This great reduction in surface area allows the plexus to negotiate the narrow passage between the clavicle and the first rib at the apex of the axilla. The brachial plexus, represented by its divisions, enters the apex of the axilla lateral to the axillary artery, the latter being the continuation of the subclavian artery. In order to offer a short profile the neurovascular bundle “spread” from medial to lateral with the axillary vein the most medial structure, followed by the axillary artery in the center and the divisions of the plexus most lateral, as shown in figure 6-3 and 6-4. Fig 6-3. Neurovascular bundle under the clavicle, left side. The soft tissue and fascias have been removed for clarity. The neurovascular bundle crosses under the clavicle with the vein most medial, the axillary artery in the center and then the divisions most most laterally. (Dissection by Dr. Franco. Copyrighted image).
Fig 6-4. Neurovascular bundle under the clavicle in cross section, left side. The alignment of the neurovascular bundle under the clavicle is shown in cross section with some of the connective tissue intact. The arrows point to the 6 divisions located lateral to the axillary artery. (Dissection by Dr. Franco. Cop yrighted image).
It is important to realize that immediately below the clavicle and before arriving at the coracoid process, the six divisions of the plexus and the origin of the three cords are located lateral to the artery and not around it (see figures 6-3 and 6-4). This is an important anatomical detail while considering different infraclavicular approaches. As the cords approach the level of the coracoid process the lateral cord remains on the lateral side while the posterior and medial cords migrate behind the artery adopting all of them the characteristic position around it from which they take their name. At this level the cords are covered superficially by pectoralis minor and pectoralis major muscles. It seems to me important to mention that the rotation of the cords behind the artery from their original lateral position is usually arrested before the medial cord reaches a true medial position with respect to the artery and before the posterior cord get to be truly posterior to it. So, a cross section of the neurovascular bundle at the level of the coracoid process reveals that the cords are not exactly located at the 3, 6 and 9 o’clock position Instead, on the right side, the lateral cord is usually in position 10 (anterolateral), the posterior cord is in position 7 (posterolateral) and the medial cord is in position 4 (posteromedial). On the left side, the lateral cord is in position 2 (anterolateral), the posterior cord in position 5 (posterolateral) and the medial cord in 75 | P a g e
position 8 (posteromedial). This means that usually there are two cords on the lateral side of the artery (lateral and posterior cords) and only one on its medial side (medial cord), making the approach from the lateral side more rational, especially during blind techniques. 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. Sometimes the musculocutaneous nerve remains attached to the median nerve until reaching the proximal arm. Brachial plexus sheath For some authors the uneven spread of local anesthetic frequently observed after a single injection in the axilla is enough evidence that the brachial plexus sheath does not exist. This is not necessarily so. On the one hand, it is clear both in the surgical suite and the anatomy laboratory, that connective tissue surrounds all types of neurovascular structures in the body, especially in more exposed areas like the axilla, the neck, the groin, etc. It is a reality that nerves and vessels are immersed in a connective tissue matrix and are not simply “cables” lying between two muscular planes. Our own published cadaver studies have provided macroscopic photographic evidence of its existence. Part of that is shown in figures 6-5 A, B and C.
Fig 6-5 A and B. Axillary sheath. Left axillary region dissection showing A: the axillary sheath intact from which the musculocutaneous nerve (MCN) is seen exiting. B: shows the same specimen after the sheath has been open. The intra sheath portion of the MCN can be seen taking off from the lateral cord (LC). Cadaver dissection by Dr Franco. Images are copyrighted. Fig 6-5 C. Axillary sheath in cross section. The axillary sheath just below the clavicle (apex) is shown with arrows as a well defined sturdy fascia surrounding the neurovascular bundle. The interior is otherwise filled with loose connective tissue. The three cords of the plexus (c) are shown lateral to the artery. Cadaver dissection by Dr Franco. Image is copyrighted.
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Ultrasound, on the other hand, has confirmed that nerves and vessels in all regions of the body, but especially in exposed places like the axilla, are embedded in a matrix of soft connective tissue surrounded by a fascial sheath. This loose connective tissue within the sheath “soaks” the local anesthetic towards areas of least resistance (i.e., along the nerves) and by doing so this soft connective tissue becomes an obstacle to free circumferential diffusion. In addition to this internal (within the sheath) factor, there are other factors outside the sheath that may also play a role in the spread of local anesthesia within it. Some of these factors have to do with the nature of the tissues through which the neurovascular bundle travels through and the pressure they exert over the sheath. In the axilla, for example, the sheath and its content are resting posteriorly over muscle and bone (scapula). So its posterior aspect is subjected to more outside pressure or resistance than its anterior aspect that is only covered by the complaint axillary fat. As a result local anesthetic, which can only move to points of least resistance, will have more difficulty spreading from the anterior aspect of the axillary sheath to its posterior aspect than vice versa and this difficulty in the spread within the sheath has nothing to do with any specific septa.
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): 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. 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 th th and dorsum of the 5 finger and dorsum of the medial side of 4 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. 77 | P a g e
Medial antebrachial cutaneous nerve (C8-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 and the origin of the divisions are located above the clavicle, therefore during a supraclavicular block the needle does not 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), therefore its penetration is unlikely during a properly performed supraclavicular block. During procedures using a needle in the supraclavicular area, 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 interscalene and supraclavicular blocks. To avoid this problem during a supraclavicular block the injection needs to be performed in the vicinity of the lower trunk or its divisions, evidenced by fingers twitch with a nerve stimulator or by injecting between the subclavian artery and the first rib when using ultrasound. In the case of interscalene block this is usually not a problem since its main indication is anesthesia/analgesia of the shoulder that does not require anesthesia of C8-T1 dermatomes. 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. size. Bigger muscle bulk through exercise does not influence the size of the muscle insertion area.
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INTERSCALENE BLOCK NERVE STIMULATOR TECHNIQUE Indications Its main indication is anesthesia or analgesia of the shoulder, including 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 space, 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 dermatomes, which include the sensory territories of ulnar, medial antebrachial cutaneous, and medial brachial cutaneous nerves (medial side of the upper extremity). 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 is placed in a semi sitting position and the space between the cricoid and thyroid cartilages (cricothyroid membrane) is located and marked as shown in figure 6-6. The patient is asked to lower his shoulders and to slightly rotate the head to the opposite side. It is important to emphasize here that the patient should rotate and not incline the head away so as to keep the midline neutral. With the midline in neutral position the intervertebral foramen looks caudal, lateral and slightly posterior. Tilting the head away from the operator, on the other hand, could align the intervertebral foramen with the needle trajectory.
Fig 6-6. Cricoid thyroid membrane. The level of the cricothyroid membrane is located by palpation and marked on the skin. (On a model with per mission). mission).
A horizontal plane that starts at the cricothyroid membrane medially and intercepts the posterior border of the SCM laterally is established, as shown in figure 6-7.
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Fig 6-7. Cricoid-SCM plane. The level of the cricothyroid membrane is projected laterally to intercept the posterior border of the SCM. (On a model with per mission). mission).
The index and middle fingers of the palpating hand are placed behind the SCM at this level pushing it slightly forward (medially), as shown in figure 6-8. This maneuver brings the palpating fingers under 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 easy to identify. This is the point of needle insertion.
Fig 6-8. Point of needle insertion. The interscalene groove is found at the intersection of the cricoid plane with the posterior border of the SCM. (On a model with per mission). mission).
Type of needle A 2.5 cm or 5cm, 22-G, insulated needle can be used. Nerve stimulator settings The nerve stimulator is set to deliver a current of 0.8-0.9 mA, at a pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). A small skin wheal is raised with 1% lidocaine or 1% mepivacaine using a small needle (ideally 27-G). Needle insertion The needle is introduced between the two palpating fingers in a medial and slightly caudal direction, but most importantly with a 20 to 30-degree posterior direction, as shown in figure 6-9.
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Fig 6-9. Needle insertion. The needle is advanced medial, caudal and posterior. (On a model with permission).
It is important to realize that this is a superficial block that should take place within the confines of the tips of the palpating fingers and not beyond them. In no circumstance the needle should be introduced further than the projection of the clavicular head of the SCM. Any distal motor twitch as well as biceps, triceps or deltoid muscles are adequate. There is some controversy in the literature as to whether a shoulder twitch is acceptable for an interscalene block. Besides the usual arm twitches, anatomical and clinical evidence support accepting deltoid twitches. Motor twitches from trapezius (spinal accessory nerve) and levator scapulae (dorsal scapular nerve) are not acceptable. For further reading on this issue please see: Silverstein W et al. Interscalene block with a nerve stimulator: A deltoid motor response is a satisfactory endpoint for successful block. Reg Anesth Pain Med 2000; 25:356-359 and accompanying editorial by William Urmey, same journal page 340-342. A twitch of the abdomen signals phrenic nerve stimulation and it is evidence that the needle is anterior to the anterior scalene. In this case the needle should be withdrawn and redirected slightly posteriorly. A motor twitch of the scapulae or trapezius muscle indicates that the position of the needle is too posterior and needs to be repositioned anteriorly. 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 of 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. The addition of lyophilized tetracaine (20 mg per 10 mL of solution) to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine, provides around 6 h of surgical anesthesia. Ropivacaine 0.5% can be used in the same volume to provide 12 h plus of anesthesia. The injection of local anesthesia is performed slowly with frequent aspirations. Also 20 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
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laryngeal nerve involvement. Characteristically this block produces also 100% of phrenic nerve block with diaphragmatic paralysis (Urmey et al, Anesth Analg, 1991). 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 to perform an interscalene block as the only anesthesia for the case. A nervous patient and a rough surgeon could be indications for interscalene analgesia combined with general anesthesia. It must be remembered that some of these procedures are performed in positions other than supine (e.g., beach chair, lateral), which can make the management of the airway, if needed, a bit more challenging. A language barrier between patient and anesthesiologist is also a relative contraindication for interscalene block as the sole anesthetic. This is a very superficial block that can be performed at 1-2 cm from the skin in most patients.
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INTERSCALENE BLOCK ULTRASOUND TECHNIQUE Indications Shoulder anesthesia and/or analgesia, including clavicle and proximal humerus. Patient position The patient is placed semi seated, with the shoulder down and the head slightly turned the opposite way, as shown in figure 6-10.
Fig 6-10. Position. The patient is semi seated, with shoulder down and head slightly rotated to the opposite side. The ultrasound machine is placed on the opposite side. (On a model with permission).
Type of needle A 2.5 cm or 5 cm, 22-G, insulated needle is what we frequently use. Type of transducer This is a superficial block for which a high frequency (8-15 MHz) linear probe is well suited. Scanning Two are the most frequent ways to scan the neck to visualize the roots of the plexus. One is to start a transverse scan over the sternocleidomastoid muscle (SCM) just lateral to the cricoid cartilage, or start more distally parallel to the clavicle and then trace the plexus proximally to the roots. In either case the probe ends in a semi transverse position (cephalad rotation) overlapping the SCM with a slight distal orientation as shown in figure 6-11.
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Fig 6-11. Probe position. To get a good perpendicular cut of the roots, the probe is slightly rotated as shown. (On a model with permission)
The image obtained at this level is shown in figure 6-12.
Fig 6-12. Interscalene image. With the probe in the position shown in fig 6-11 it is possible to visualize part of the SCM, ant and middle scalene muscles and the proximal roots of the plexus. chive) (Author’s ar chive)
Needle insertion
The needle can be advanced in plane from medial to lateral, or lateral to medial, or out of plane usually from cephalad to caudal. It is our preference to insert the needle in plane from lateral to medial as shown in figures 6-13 and 6-14.
Fig 6-13. Needle insertion. The needle is introduced in plane from lateral to medial. (On a model with permission)
Fig 6-14. US image. Vertical arrows show the needle while the two horizontal arrows show part of the hypoechoic spread of local anesthetic around the plexus roots. (Author’s archive)
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This technique resembles Winnie’s classical interscalene approach. With the needle under direct visualization the injection is performed in the proximity of C6 root. The spread of local anesthetic should expand the interscalene space and bathe C5-C6 and C7 roots, as shown in figure 6-14. If the spread is insufficient around a particular root the needle is repositioned accordingly for a new injection. Local anesthetic and volume We use between 20-30 mL of local anesthetic of the same kind used for nerve stimulation techniques. Side effects and complications The side effects and complications are essentially the same described for nerve stimulation techniques. It is possible that ultrasound techniques, with a more targeted injection and potentially smaller volumes, may theoretically decrease the incidence of side effects, but this remains to be proven.
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SUPRACLAVICULAR BLOCK NERVE STMULATOR TECHNIQUE Indications This block is indicated for any surgery on the upper extremity distal to the shoulder or for analgesia of the entire upper extremity. 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 by some as more difficult to learn than other upper extremity blocks and historically it has been associated with a higher risk of pneumothorax. The literature cites pneumothorax rates between 0.5-6.1 percent. However with good anatomy and meticulous technique we have been able to practically eliminate this risk. A supraclavicular block is usually associated with a short onset, dense anesthesia and high success rate. As we discussed it in the anatomy section, this is due to the compact arrangement of the plexus at the level of trunks and divisions. Because of these favorable characteristics, the supraclavicular block has been called the “spinal of the upper extremity”. We perform our own variation of the supraclavicular block, a very anatomical approach that starts by determining the pleura boundaries as the first step. This allows us to take advantage of such extraordinary block while limiting its potential drawbacks. Our experience to late 2009 includes more than 5,000 supraclavicular blocks without ever having demonstrated a single pneumothorax. A common question posed to us is whether we perform routine chest X-rays after a supraclavicular block. The answer is no. In fact we only do an X-ray when the clinical situation merits it (e.g., an unusually difficult technique and or symptomatic patient). Traditionally our anesthesiology textbooks have left the impression that a pneumothorax following a supraclavicular block has a late onset, making the technique a bad choice for outpatients. Our review of the literature fails to demonstrate this. In fact most of the cases of pneumothorax associated with supraclavicular block published in the literature, have been diagnosed within a few hours after the block and most of them have been investigated because of the patients’ early symptoms. We perform this technique with great success in all kinds of patients, including same day surgery and trauma patients. Some history of the supraclavicular approach The supraclavicular block was introduced into clinical practice in Germany by Kulenkampff in 1911. A publication of his technique appeared later in the English literature in 1928. Kulenkampff accurately described the plexus as being more compacted in the neighborhood of the subclavian artery, where he rightly believed that a single injection could provide could 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
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T3, carried an inherited risk for pneumothorax that would be responsible for the technique falling into disfavor. Albeit with several modifications, the supraclavicular approach remained a popular choice until the early 1960’s. Eventually, the combined effect of pneumothorax fear 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 approaches in regional anesthesia. 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. His 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 issue carried a paper by Brand and Papper out of New York, comparing axillary and supraclavicular techniques in their hands. This article is the source of the 6.1% pneumothorax rate frequently quoted for supraclavicular block. The authors were determined to prove that the axillary block was safer and better than the supraclavicular block. They succeeded by not only producing the highest percentage of pneumothorax (6.1%), but the highest number (14 cases) for an individual study. This study should be considered an aberration. In retrospect these two articles could be considered the turning point at which the axillary route became the preferred approach here in the United States and the rest of the world. With some exceptions this is still true today. Fortunately ultrasound in regional anesthesia has caused a renewed interest in this approach and we could not be happier. The supraclavicular technique with its rapid onset, density, high success rate along with large area of anesthesia are highly desirable. These good characteristics are, according to David Brown and colleagues, colleag ues, “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 in the semi sitting position, the ipsilateral shoulder down and the head turned to the opposite side, as shown in figure 6-15. The arm to be blocked is flexed at the elbow and, if possible, the wrist is supinated to easily detect a twitch of the fingers.
Fig 6-15. Patient position. The patient is semi seated with the head of the bed elevated 30 degrees. The head of the patient is turned away, the shoulder is down and the arm is flexed at the elbow and supinated at the wrist. (On a model with permission).
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The point at which the clavicular head of the SCM muscle inserts in the clavicle is then identified, as shown in fig 6-16. A parasagital (parallel to the midline) plane at this level determines an “unsafe” zone medial to it, where the risk of pneumothorax is high and a lateral zone that is safer.
Fig 6-16. Lateral head of SCM. The most lateral insertion of the SCM on the clavicle is found and marked with an arrow. Crossing this plane medially increases the risk of pneumothorax. (On a model with per mission).
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 SCM on the clavicle to be safely away from the pleural dome, but not too far to miss the trunks and the plexus completely. 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 6-17.
Fig 6-17. Safety margin. A safety margin of 1” (2.5 cm) lateral to the insertion of the SCM on the clavicle is marked on the skin. (On a model with permission).
This is only an orientation point that usually will coincide with the midpoint of the clavicle in an adult patient. At this level the brachial plexus is usually easily palpable, either as a groove or as some type of bump(s) . This is usually called “interscalene groove”, groove”, but the interscalene groove only exists high in the C5-C6 level. The groove is lost more distally as the scalene muscles diverge from each other in the frontal and sagittal planes. The palpation of the plexus is what determines the actual point of needle entrance and not a fixed distance. The plexus can be palpated a few mm medial or lateral to the orientation point, but never too far from it. The palpating finger is placed parallel to the clavicle and the point of needle entrance is located immediately cephalad to it, as shown in figure 6-18.
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Fig 6-18. Orientation arrows. The medial arrow pointing up shows the lateral insertion of SCM (pleura’s lateral boundary). The lateral arrow pointing caudally shows the needle entrance point. The two lateral arrows pointing at each other show the needle trajectory (parallel to the patient’s midline). (On a model with permission).
Type of needle A 5cm, 22-G, insulated needle is used for this technique. Nerve stimulator settings The nerve stimulator is set to deliver a current of 0.8-0.9 mA, at a pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). A small skin wheal is raised with 1% lidocaine or 1% mepivacaine using a small needle (ideally 27-G). Needle insertion The needle is inserted first anteroposterior (toward the bed) with a 30 degree caudal orientation, as shown in figure 6-19, for a distance of a few mm and up to 1.5 cm, depending on the amount of subcutaneous tissue. After a short distance, a twitch of the upper trunk (shoulder) is usually found as evidence that the needle is approaching the frontal plane of the plexus.
Fig 6-19. Needle insertion. The needle is first introduced in a posterior direction (toward the bed) with a 30 degree caudal orientation. (On a model with permission).
The direction of the needle is then changed from anteroposterior to caudal, advancing it parallel to the midline (and parallel to the most lateral pleural boundary), with a slight (10 degrees) posterior orientation, as shown in figure 6-20.
Fig 6-20. Direction of the needle. The needle is then advanced caudad, parallel to the midline, with a slight posterior orientation. (On a model with permission).
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The reference to the midline is easy to ascertain and avoids confusion. The use of other landmarks (e.g., nipple) provides lesser accuracy because of variability among patients. The needle is advanced caudally with a slight posterior angle to match the slight posterior rotation of the plexus (the upper trunk is the most anterior and the inferior trunk the most posterior). Because the trunks are physically contiguous, as the needle is advanced, a twitch of the upper trunk (shoulder) should be followed by one from the middle trunk (pectoralis, triceps, supination, pronation) and finally a twitch from the lower trunk (wrist and fingers). The goal of the technique is to produce an isolated muscle twitch of the fingers. Wrist flexion and extension are also acceptable responses, but supination or pronation or any other more proximal motor twitches are not. If after advancing the needle the motor twitch of the shoulder disappears and no twitch is elicited from the middle trunk, it usually means that the angle of insertion of the needle is not matching the orientation of the trunks, and that the tip of the needle is wandering away from the trunks (usually anteriorly). The needle should be slowly withdrawn until the original twitch is elicited once again, 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 should be reassessed starting with the nerve stimulator and its connections and determination of landmarks. On the other hand, when a twitch from the brachial plexus is being elicited the depth of needle insertion is less important as such motor twitch reveals that the needle is still in close proximity to the plexus. Side effects and complications Besides the common complications accompanying any block, the supraclavicular technique can also be followed by Horner’s syndrome, hoarseness and phrenic nerve 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 (PFTs) or subjective symptoms of respiratory difficulty. This is our experience too. In the issue of pneumothorax, I already mentioned that the literature cites a risk of 0.5% to 6.1%, the latter being an aberration. A careful and meticulous technique should carry a minimal risk of pneumothorax. In our long experience including thousands of cases in all sorts of patients we have never demonstrated a case of pneumothorax. 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 location of 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.
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When using a nerve stimulator technique, 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 and gentle aspirations. This technique provides 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.
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SUPRACLAVICULAR BLOCK ULTRASOUND TECHNIQUE Indications Anesthesia and/or analgesia for any procedure on the upper extremity distal to the shoulder. Patient position The patient is placed in the semi seated position as shown in figure 6-21.
Fig 6-21. Position. The patient is placed semi seated with the shoulder down and the head turned the opposite way. (On a model with permission).
Type of needle A 5cm, 22-G, insulated needle is used. Type of transducer This is also a superficial block for which a high frequency (8-15 MHz) is used. Scanning We usually start scanning medially, over the sternocleidomastoid muscle, right above the clavicle, as shown in figure 6-22.
Fig 6-22. Probe position, first stage. The probe is place over the SCM and above and parallel to the clavicle. (On a model with permission).
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At this level we get to see the dome of the pleura and above it, the subclavian vein at that point where it is joining the internal jugular vein to form the brachiocephalic vein, as shown in figure 6-23.
Fig 6-23. Scanning, first image. With the probe over the SCM the subclavian vein and pleural dome can be visualized. (Author’s archive).
The probe is then slid laterally towards the midpoint of the clavicle, as shown in figure 6-24,
Fig 6-24. Probe position, second stage. The probe is moved laterally to visualize the plexus as it passes over the 1st rib. (On a model with ermission).
At this level a cross section of the subclavian artery, the first rib and plexus can be visualized, as shown in figure 6-25.
Fig 6-25. Scanning the plexus above the clavicle. The subclavian artery (SA) is seen above the first rib, which is shown with three arrows pointing up. A small arrow pointing down shows the pleura while the larger single arrow shows the position of the divisions of the plexus. (Author’s archive).
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Needle insertion The needle is advanced in plane, from lateral to medial, as shown in figure 6-26. The entrance point is located at about 1 cm away from the probe to decrease the angle of insertion and improve the chances of needle visualization.
Fig 6-26. Needle insertion. The needle is advanced in plane, from lateral to medial. (On a model with permission).
The needle is then slowly advanced under direct visualization, towards the angle formed by the first rib and the subclavian artery, as shown in figures 6-27 A and B.
Fig 6-27, A and B. Needle insertion. The needle is slowly brought behind the subclavian artery (AA) and above the first rib. (Author’s archive).
Intermittent injections of small amounts of local anesthetic solution helps keep contact with the tip of the needle as it advances and gently expands the volume of the connective tissue surrounding the nerves, what has been called “hydro dissection”. This contributes to clear a path for the needle decreasing the chances of inadvertent neural puncture. The goal of the supraclavicular technique is to see the spread of local anesthetic reaching the angle between the first rib and the subclavian artery, as shown in figure 628.
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Fig 6-28. Injection. The local anesthetic spread should be seen reaching the angle formed by the 1st rib (vertical arrows pointing up) and the subclavian artery (SA). The local anesthetic is seen as a hypoechoic (dark) shadow projecting from the tip of the needle. (Author’s archive).
Local anesthetic and volume For single shot techniques in adults, 30 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 it rarely persists for more than 2 h after block resolution. The addition of 2 mg/mL of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine, prolongs the duration of surgical anesthesia to 4-6 hours. Ropivacaine 0.5% can be used in the same volume to provide more than 12 h of anesthesia. Also 20-30 mL of 0.2% ropivacaine can be used to provide postoperative analgesia for surgery performed under general anesthesia.
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INFRACLAVICULAR BLOCK NERVE STIMULATOR TECHNIQUE Indications This block can provide anesthesia/analgesia of a large area of the upper extremity including the elbow, especially if performed proximally near the apex of the axilla. It is considered a good approach for continuous techniques because it offers more stability than other more mobile locations. Point of contact of the needle with the brachial plexus The needle approaches the plexus at the level of the cords, or even divisions if the block is performed proximally, closed to the clavicle. Main characteristics The infraclavicular block could be considered an axillary block in which the needle enters the axilla through its anterior wall (pectoralis muscles), instead of through its base. The infraclavicular space of the anesthesiologists corresponds to part of the axillary pyramid of the anatomists. With the arm in adduction it is represented on the skin by a triangular area whose base is superior (clavicle), a medial wall formed by the projection on the skin of the thoracic cage and a lateral wall formed by the medial side of the upper arm. Depending on the patient’s amount of subcutaneous tissue and/or muscle this block can be deep. Patients should be adequately sedated. It is widely recommended when using a nerve stimulator to obtain a distal twitch in the hand or wrist and to avoid either a biceps twitch (musculocutaneous nerve or lateral cord) or pronation of the forearm (lateral cord). This recommendation is based on clinical experience. A biceps twitch could be the result of musculocutaneous nerve stimulation, outside the sheath, or from lateral cord stimulation inside the sheath. Because the operator cannot accurately distinguish one from the other, this response is unreliable. It is likely that a twitch from the posterior cord (elbow, wrist and or finger extension) could be best, because the posterior cord is located at about the same distance from the other two, and the spread of local anesthetic from this central location might be more even. There could be another good reason to inject behind the artery, although it may be more difficult to get there. Because the posterior structures (including the posterior cord) are more closely packed, the spread of local anesthetic from anterior to posterior may be more difficult than from posterior to anterior. Ultrasound, with visualization of the axillary artery and the cords around it, makes this injection easier to accomplish. Different 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 40 volunteers by Wilson, Brown et al, and published in Regional Anesthesia in 1998. This is the technique we most frequently perform when using nerve stimulation.
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Patient position and landmarks The patient is placed semi seated with the ipsilateral shoulder down. The arm is slightly abducted 30-45 degrees, as shown in figure 6-29, to bring the neurovascular bundle away from the thoracic cage and decrease the chance of pneumothorax.
Fig 6-29. Patient position. The patient lays semi seated with shoulders down and the arm to be blocked in slight abduction. (On a model with permission).
As the neurovascular bundle follows the arm its relationship to the coracoid process is pretty much maintained. The coracoid process is found by palpation at the level of the deltopectoral groove (junction between the middle third with the lateral third of the clavicle), about 2 cm below the clavicle, and marked on the skin, as shown in figures 6-30 and 6-31.
Fig 6-30. Coracoid palpation. The coracoid is found below the clavicle in the deltopectoral groove. (On a model model with ermission ermission .
Fig 6-31. Coracoid marking. The position of the coracoid is marked on the skin. (On a model with permission).
Needle insertion point The point of needle entrance is marked 2 cm caudal and 2 cm medial to the coracoid process as shown in fig 6-32.
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Fig 6-32. Needle entrance point. Two cm caudal and two cm medial from the coracoid process. (On a model with permission).
Type of needle It is possible to use sometimes a 5cm, 22-G insulated needle, but a 10cm, 21-G insulated needle is usually necessary. Nerve stimulator settings The nerve stimulator is set to deliver a current of 0.8-0.9 mA, pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion The needle attached to the nerve stimulator is advanced in the anteroposterior direction, towards the bed, as shown in figure 6-33.
Fig 6-33. Needle insertion. The needle is introduced from anterior to posterior. (On a model with ermiss ermission ion .
Before entering in contact with the plexus the needle passes through pectoralis major and pectoralis minor muscles producing a visible local twitch. The brachial plexus is found deep to them. If not response from the plexus is obtained, the needle is redirected caudal (most of the times) or cephalad, but maintaining the same parasagital plane without medial or lateral deviation. Local anesthetic and volume The nerve stimulator-guided infraclavicular technique usually requires a relatively high volume of local anesthetic for better results. Usually 40 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. The addition
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of 2 mg/mL of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine provides 4-6 h of surgical anesthesia. Ropivacaine 0.5% can be used in the same volume for more than 12 h of anesthesia. Also 20-30 mL of 0.2% ropivacaine can be used to provide postoperative analgesia for surgery performed under general anesthesia. Side effects and complications Muscle pain and hematomas, which can be large in size, can happen. Pneumothorax can occur due to injury of the pleura through an intercostal space.
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 than other more superficial blocks. The junction between lateral and middle third of the clavicle can be used to locate the deltopectoral groove and the coracoid process. Placing the arm in slight abduction (30-40 degrees) brings the neurovascular bundle away from the thoracic cage (it follows the arm) and decreases the chance of pneumothorax.
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INFRACLAVICULAR BLOCK ULTRASOUND TECHNIQUE Indications The same indications mentioned for nerve stimulation techniques, basically anesthesia/analgesia of elbow, forearm wrist and hand. Two main infraclavicular techniques Ultrasound introduces a degree of flexibility to our techniques of regional anesthesia that we did not have before. It certainly gives the operator the chance to choose the best needle path based on the anatomy and the ultrasound image obtained, without necessarily having to conform strictly to any particular technique already described. When using ultrasound in the infraclavicular area I distinguish two main approaches, a proximal one just under the clavicle and a more distal one at the level of the coracoid process. As I mentioned in the anatomy section, the brachial plexus crosses under the clavicle as divisions before forming three cords. The divisions and the proximal trajectory of the cords below the clavicle are located lateral to the axillary artery. When the cords approach the coracoid process they rotate and surround the artery to take the position from which they get their names. Based on these two different dispositions of the plexus with respect to the axillary artery I will describe two techniques. Patient position We perform both techniques with the patient in the semi seated position with the shoulder on the side to be blocked down and the arm in abduction of about 45 degrees, as shown in figure 6-34. Abducting the arm improves the ultrasound image of the neurovascular bundle, perhaps by stretching it and bringing it closer to the anterior wall.
Fig 6-34. Patient position. The patient is semi seated, shoulder down, arm abducted. (On a model with permission).
Type of needle A 5cm, 22-G, insulated needle can be used in some patients, but it is usually necessary to use a 10cm, 21-G, insulated needle due to the depth of the neurovascular bundle at this location. Because the needle crosses through muscle, good sedation is important as well as injection of local anesthetic in the intended needle path to keep the patient comfortable.
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PROXIMAL INFRACLAVICULAR TECHNIQUE Type of transducer Depending on the thickness of the patient’s chest wall the operator can use a linear high frequency (8-15 MHz) probe or a curved low frequency (3-7 MHz) one. Scanning For this more proximal approach we place the transducer parallel and immediately below to the midpoint of the clavicle, as shown in figure 6-35.
Fig 6-35. Proximal scanning, left side. The transducer is placed parallel to the midpoint of the clavicle and immediately below it. (On a model with ermission).
The image obtained at this proximal level is a cross section of the neurovascular bundle as it aligns under the clavicle in a formation that has the axillary vein as the most medial structure, followed by the axillary artery in the center and the divisions of the plexus most laterally, as shown in figure 6-36.
Fig 6-36. Proximal scanning, left side. At this proximal level pectoralis major (Pec major) is the main muscle seen superficial to the neurovascular bundle. Pectoralis minor is located distally to this US section. Among the neurovascular bundle structures the axillary vein (AV) is the most medial, followed by the axillary artery (AA) and then the divisions of the plexus most laterally. (Author’s archive).
Needle insertion The needle can be advanced out of plane from caudal to cephalad, but we usually prefer an in plane technique from lateral to medial, as shown in figure 6-37.
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Fig 6-37. Needle insertion, left side. The needle is introduced in plane from lateral to medial. (On a model with ermission).
Figures 6-38 A, B and C, show a sequence of ultrasound images showing needle insertion and injection.
Figure 6-38; A, B and C. Needle insertion/injection, left side. A (left): the divisions of the plexus are shown surrounded by a fascial sheath lateral to the axillary artery (AA); B (center): the shadow of the needle path (pointed by arrows) is barely seen as the needle comes in at a 45 degree angle. The two smaller arrow heads point to the indentation of the fascia produced by the piercing needle; C: the spread of local anesthetic is seen as a hypoechoic shadow pointed by a large arrow and the resulting expanded sheath is shown with the smaller arrows. (Author’s archive)
CORACOID INFRACLAVICULAR TECHNIQUE This technique is performed around the coracoid, but as opposed to the nerve stimulation technique the level is not dictated by a fixed measurement with respect to the coracoid, but instead by an optimal ultrasound image of the axillary artery and the surrounding cords. Type of transducer A linear high frequency (8-15 MHz) or a curved low frequency (3-7 MHz) probe is used depending on the thickness of the patient’s thoracic wall. Scanning For this more distal approach we place the transducer in an oblique fashion in the mid pectoral region, as shown in figure 6-39. This probe rotation is needed to get a better cross section of the neurovascular bundle, which is traveling diagonally in the infraclavicular region.
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Fig 6-39. Coracoid level scanning, right side. The transducer is placed in an oblique fashion to get a perpendicular cut of the neurovascular bundle at the level of the coracoid process. (On a model with
The ultrasound image obtained at this level is shown in figure 6-40. At this level the cords of the plexus have already rotated behind the axillary artery and adopted their arrangement around it from which they take their names, medial, posterior and lateral.
Fig 6-40. Coracoid level scanning, right side. With the probe at the level of the coracoid process the neurovascular bundle appears under both pectoralis muscles. The axillary vein (V) is more medial, close to the chest wall, while the axillary artery (A) is more lateral, surrounded by the three cords, lateral (L), posterior (P) and medial (M). (Author’s archive).
Needle insertion As it is the case with the more proximal approach, the needle can be inserted out of plane, from caudal to cephalad, but we usually prefer to advance it in plane, from lateral to medial (superior to inferior), as shown in figure 6-41.
Fig 6-41. Needle insertion, right side. The needle is introduced in plane, from lateral (superior) to medial (inferior). (On a model with permission).
Clinical pearls The proximal infraclavicular approach is a block of the divisions of the plexus and as such it can resemble a supraclavicular block in onset and density of anesthesia.
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AXILLARY BLOCK NERVE STIMULATOR TECHNIQUE Indications It is best suited for anesthesia/analgesia of the upper extremity 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 brachial plexus block, but rather a block of its terminal branches. The larger surface area that the branches as a whole occupy and the tendency for the local anesthetic to follow the paths of low resistance along individual nerves affect the circumferential spread of the local anesthetic within the sheath (please see discussion on axillary brachial plexus sheath in the anatomy section). A single injection technique is an option, but multiple injections have shown to increase the success rate at this level. If a single injection is to be attempted, the operator needs to specifically target the nerve feeding the surgical area. If the surgical area involves more than one terminal nerve, the single injection technique should be performed in the proximity of the radial nerve because, as mentioned in the anatomy discussion, the local anesthetic solution tends to spread inside the sheath more easily from back to front that vice versa. In addition, my observations in the anatomy lab show that better circumferential spread of local anesthetic may be obtained with a slight elevation of the elbow, because this maneuver releases some of the stretching of the neurovascular bundle. Some authors advice to perform the block high in the axilla to improve its overall success. 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 sheath, but since its take off is variable the operator could never be certain. I believe that a better strategy is to start the axillary block by first blocking the musculocutaneous nerve in the proximal arm and then complete the block according to what is needed. Although some variability exists, usually the median nerve is superficial (anterior) to the axillary artery, following its same direction; the ulnar nerve (and medial brachial/antebrachial cutaneous nerves) 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. st I believe that in the 21 century, with the variety of tools at our disposal, there is no good reason to perform a trans axillary technique. Patient position and landmarks The patient is supine, the arm is abducted to about 80-90 degrees and the elbow is slightly elevated 20-30 degrees by using a small pillow or folded blanket. The biceps muscle is identified by visualization and/or palpation. The coracobrachialis muscle is found immediately under it (posterior). While biceps is highly mobile the coracobrachialis is palpated as a thick poorly movable mass. The pulsation of
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the axillary artery is found immediately under the coracobrachialis. Sometimes it helps to displace the latter slightly anterior to feel the pulsation of the artery. Figure 6-42 shows the arm position in abduction with a small pillow under the elbow and the trajectory of the axillary artery marked in blue.
Fig 6-42. Patient position and axillary artery marking. The arm is abducted about 80° to 90°, the elbow is elevated slightly with a small pillow and the axillary artery is marked. (On a model with permission).
Type of needle This is usually a superficial block, even in obese patients. A 5cm, 22-G, insulated needle usually suffices. Single injection axillary block As I mentioned before, evidence shows that success rate in the axillary region increases with 2 and 3 injection techniques as opposed to a single injection. If a single injection technique is employed the “epicenter” of the injection should occur at the nerve that is more relevant to the surgical site. If more than one nerve is involved in the innervation of the surgical site, the single injection technique should be performed preferably in front of the radial nerve. The volume of local anesthetic needed for a single injection technique is 40 to 50 mL. If more than one injection is performed the volume should be divided accordingly. If only one nerve is needed 5 mL of local anesthetic solution is enough for anesthesia. A solution of 1.5% mepivacaine plus 1:400,000 epinephrine provides 3-4 hr of anesthesia. If longer anesthesia is desired 0.5% ropivacaine with epinephrine provides 12 hr plus of anesthesia. For analgesia 0.2% ropivacaine is adequate.
In order to perform a targeted injection of a specific nerve in the axilla it is necessary to know how to block each individual nerve. The following is a description of each technique. MUSCULOCUTANEOUS NERVE BLOCK The musculocutaneous nerve originates from the lateral cord (it can take off from the median nerve already in the arm) and because of its uncertain take off level we like to block it first. Nerve stimulator setting The nerve stimulator is set to deliver a current of 0.8-09 mA, pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). A small skin wheal is raised with 1% lidocaine or 1% mepivacaine using a small needle, ideally 27-G.
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Needle insertion 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, advancing it between biceps and coracobrachialis, as shown in figure 6-43.
Fig 6-43. Blocking the musculo cutaneous nerve. The needle is introduced under the biceps perpendicular to the main axis of the arm. (On a model with permission).
Type of response As the needle approaches the musculocutaneous nerve a motor twitch of biceps with flexion of the elbow is obtained. The current is reduced to 0.5 mA and, if a response is still visible at this level, the injection is started. MEDIAN NERVE BLOCK
The median nerve is most frequently located anterior (superficial) to the axillary artery running in the same direction, making it a very superficial block. Nerve stimulator settings The nerve stimulator is set to deliver a current of 0.8-09 mA, pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). A small skin wheal is raised with 1% lidocaine or 1% mepivacaine using a small needle, ideally 27-G. Needle insertion Using the mark of the axillary artery on the skin as a reference, the needle is introduced very tangential to the skin (shallow angle), in the same direction of the artery, as shown in figure 6-44.
Fig 6-44. Median nerve block. The needle is introduced in reference to the axillary artery with a very shallow angle and in the same direction than the artery. (On a model with per mission). mission).
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It is better to mark the course of the artery on the skin than to keep the fingers on the pulse to avoid bringing the artery even closer to the skin and increasing the chances for accidental artery puncture. ULNAR NERVE BLOCK
The ulnar nerve is located immediately medial to the artery, slightly deeper than the median nerve. It gives sensory innervation to the medial side of the hand. Because the medial brachial and the medial antebrachial cutaneous nerves run along with the ulnar nerve on the medial side of the axillary artery, the ulnar nerve technique is performed for anesthesia of the medial arm and medial forearm. Nerve stimulator settings The nerve stimulator is set to deliver a current of 0.8-09 mA, pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion Using the mark of the axillary artery on the skin as a reference, the needle is directed slightly medial to the artery, as shown in figure 6-45.
Fig 6-45. Ulnar nerve block. The needle is introduced slightly medial to the line representing the axillary artery. Notice the small difference in the angle of insertion compared to the median nerve block. (On a model with permission).
RADIAL NERVE BLOCK
The radial nerve is most frequently located posterior (deeper) to the axillary artery. It is the largest of the terminal branches of the plexus. Nerve stimulator setting The nerve stimulator is set to deliver a current of 0.8-09 mA, pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion The operator operator uses two fingers of one hand as “hooks” to slightly displace the artery out of the way in order to reach the radial nerve located posterior to it. The needle is inserted posterior with a 30 degree cephalad orientation, as shown in figure 6-46.
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Fig 6-46. Radial nerve block. The axillary artery is displaced towards the biceps to gain entrance to its posterior aspect. The needle is then introduced in reference to the mark on the skin with a 30 degree cephalad orientation. (On a model with permission).
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 indicated 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 deeper planes of the arm. Two and three injection techniques have proven more successful, but if a single injection is preferred this injection should be in front of the nerve most responsible for the sensory innervation of the surgical site. If more than one nerve is involved the injection should be performed in front of the radial nerve.
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AXILLARY BLOCK ULTRASOUND TECHNIQUE Indications The same indications mentioned for the nerve stimulation technique. Patient position The patient is semi seated with the arm in abduction and the elbow flexed, as shown in figure 6-47.
Fig 6-47. Patient position. The patient is semi seated, with the arm abducted and the elbow flexed. (On a model with permission).
Type of needle This is a superficial block for which a 5cm, 22-G, insulated needle suffices. Type of transducer We use a high frequency (8-15 MHz) linear probe. Scanning The probe is placed across the neurovascular bundle in the proximal part of the arm, as shown in figure 6-48.
Fig 6-48. Scanning. The probe is place perpendicular to the main axis of the neurovascular bundle. (On a model with permission).
At this level the neurovascular bundle of the axilla is usually very superficial and the terminal nerves can be seen surrounding the axillary artery. The median nerve is usually superficial (anterior) to the artery, the ulnar nerve is medial and somewhat posterior, and the radial nerve is posterior, as shown in figure 6-49.
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Fig 6-49. Terminal branches. The axillary sheath has been removed to show the relative location of the nerves with respect to the axillary artery. MACN: medial antebrachial cutaneous nerve; axi: axillary nerve. Cadaver dissection by Dr Franco. Im Ima e is is co co ri hted.
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 traced from its origin in the lateral cord proximally to its location between biceps and coracobrachialis distally. 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. An image of the neurovascular bundle of the axilla in cross section is shown in figure 6-50.
Fig 6-50. Axillary scanning. With the probe across the axilla the axillary artery (AA) is seen surrounded by three main nerves, median (M), Ulnar (U) and Radial (R). Also seen is Musculocutaneous nerve (MC), axillary vein (AV) and some muscles. (Author’s archive).
Needle insertion The needle is advanced in plane from lateral to medial, as shown in figure 6-51.
Fig 6-51. Needle insertion. The needle is advanced in plane from lateral (superior) to medial (inferior) and aimed toward the desired nerve. (On a model with permission).
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We usually block first the musculocutaneous nerve located in between biceps and coracobrachialis. To target this nerve the needle needs to be inserted at an angle of 30-45 degrees. Then the rest of the terminal branches are targeted as needed. These branches are more superficial so they need a much smaller angle of insertion, which facilitates needle visualization. Local anesthetic and volume Because the nerves can be targeted individually it is possible to inject about 5 mL of local anesthetic solution per nerve until all the needed nerves are completely surrounded by it, usually requiring a total volume of 20-30 mL. For anesthesia we use 1.5% mepivacaine plus 1:400,000 epinephrine, which gives 3-4 hours of surgical anesthesia. For more prolonged anesthesia 0.5% ropivacaine with epinephrine can be used. For postoperative analgesia we recommend 0.2% ropivacaine. Side effects and complications The most common complication at the axillary level is hematoma at the site, but ultrasound provides a good visualization of vessels and nerves at this location making this occurrence more rare.
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References
1. Brown DL. Brachial plexus anesthesia: an analysis of options. Yale J Biol Med 1993; 66: 415-431 2. Winnie AP. Interscalene brachial plexus block. Anesth Analg 1970; 49: 455-466 3. Kulenkampff D, Persky MA. Brachial plexus anesthesia. Ann Surg 1928; 87: 883891 4. Winnie AP, Collins VJ. The subclavian perivascular technique of brachial plexus anesthesia. Anesthesiology 1964; 25: 353-363 5. Franco CD, Vieira Z. 1,001 subclavian perivascular brachial plexus blocks: success with a nerve stimulator. Reg Anesth Pain Med 2000; 25: 41-46 6. Franco CD. The subclavian perivascular block. Tech Reg Anesth Pain Med 1999; 3: 212-216 7. De Andres J, Sala-Blanch X. Peripheral nerve stimulation in the practice of brachial plexus anesthesia: a review. Reg Anesth Pain Med 2001; 26: 478-483 8. Greenblatt Gm, Denson GS. Needle nerve stimulator-locator: nerve blocks with a new instrument for locating nerves. Anesth Analg 1962; 41: 599-602 9. Hadzic A, Vloka J, Hadzic N, et al. Nerve stimulators used for peripheral nerve blocks vary in their electrical characteristics. Anesthesiology 2003; 98: 969-974 10. Passannante AN. Spinal anesthesia and permanent neurologic deficit after interscalene block. Anesth Analg 1996; 82: 873-874 11. Urmey WF, Grossi P, Sharrock NE, Stanton J, Gloeggler PJ. Digital pressure during interscalene block is clinically ineffective in preventing anesthetic spread to the cervical plexus. Anesth Analg 1996; 83: 366-370 12. Silverstein WB, Saiyed M, Brown AR. Interscalene block with a nerve stimulator: A deltoid motor response is a satisfactory endpoint for successful block. Reg Anesth pain Med 2000; 25: 356-359 13. Urmey WF, Talts KH, Sharrock NE. One hundred percent incidence of hemidiaphragmatic paresis associated with interscalene brachial plexus anesthesia as diagnosed by ultrasonography. Anesth Analg 1991; 72: 498-503 14. Urmey WF. Interscalene block: The truth about twitches (editorial). Reg Anesth pain Med 2000; 25: 340-342 15. Brand L, Papper EM. A comparison of supraclavicular and axillary techniques for brachial plexus blocks. Anesthesiology 1961; 22: 226-229 16. Brown DL. Atlas of regional anesthesia. Philadelphia, PA: W.B. Saunders, 1992 rd 17. Mulroy MF. Regional anesthesia: An illustrated procedural guide. 3 edition. Philadelphia, PA; Lippincott Williams & Wilkins 2002 18. Urmey WF, Stanton J. Inability to consistently elicit a motor response following sensory paresthesia during interscalene block administration. Anesthesiology 2002; 96: 552-554 19. Neal JM, Moore JM, Kopacz DJ, Liu SS, Kramer DJ, Plorde JJ. Quantitative analysis of respiratory, motor, and sensory function after supraclavicular block. Anesth Analg 1998; 86: 1239-1244 20. 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: 1167-1171 112 | P a g e
21. Franco CD, Gloss FJ, Voronov G, Tyler SG, Stojiljkovic LS. Supraclavicular block in the obese population: An analysis of 2020 blocks. Anesth Analg 2006; 102: 1252-1254 22. Perlas A, Chan V: Ultrasound-assisted nerve blocks. In: Textbook of Regional Anesthesia, Anesthesia, Hadzic A (ed). New York, McGraw Hill, 2007, pp 663-672 23. Franco CD, et al. Gross anatomy of the brachial plexus sheath in human cadavers. Reg Anesth Pain Med 2008; 33: 64-69 24. Neal JM, Gerancher JC, Hebl JR, Ilfeld BM, McCartney CJL, Franco CD, Hogan QH. Upper Extremity Regional Anesthesia: Essentials of Our Current Understanding. Reg Anesth Pain Med 2009; 34: 134-170
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CHAPTER 7 LOWER EXTREMITY NERVE BLOCKS
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LOWER EXTREMITY BLOCKS
The innervation of the lower extremity comes from the lumbar and sacral plexuses. The different nerve elements of the lower extremity run more distant from each other than those of the upper extremity, without having a point of convergence like the one at the level of the brachial plexus trunks. Therefore, no single peripheral block technique is able to provide anesthesia of the whole lower extremity. This anatomical fact, combined with the high success of neuraxial anesthesia, has traditionally affected the popularity of lower extremity peripheral nerve blocks. The introduction of low molecular weight heparin (LMWH) in the United States in the early 1990s produced a renewed interest in lower extremity nerve blocks because of the increased risk of epidural hematoma after neuraxial anesthesia in patients receiving LMWH. The use of ultrasound in regional anesthesia has also been a major reason for the increased popularity of all sort of peripheral nerve blocks. Anatomy Lateral femoral cutaneous nerve It is an exclusively sensory nerve originating from the ventral rami of spinal nerves L2-L3. It appears in the pelvis, lateral to the psoas muscle, caudal to the ilioinguinal nerve. It runs anteriorly 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, as shown in figure 7-1 and 7-2. It provides sensory innervation to the lateral thigh.
Fig 7-1. Lateral femoral cutaneous nerve (LFCN), left side. The LFCN shown with arrows perforates the fascia lata below the inguinal ligament to become a superficial nerve. Cadaver dissection by Dr Franco. Image is copyrighted.
Femoral nerve It is a motor and sensory nerve derived from the posterior divisions of the ventral rami of spinal nerves L2-L3-L4. In the pelvis it is also located lateral to the psoas muscle, in the cleavage between psoas and iliacus muscles. As it passes under the inguinal ligament the nerve is superficial to the combined iliopsoas muscle. Under the inguinal ligament the femoral nerve has the femoral artery medial to it, while the femoral vein is located medial to the artery (VAN from medial to lateral), as shown in figure 7-2.
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Fig 7-2. Femoral nerve, left side. The femoral nerve (FN) passes under the inguinal ligament lateral to the femoral artery (A). Also shown are the femoral vein (V) and the LFCN pointed with arrows. Cadaver dissection by Dr Franco. Image is copyrighted.
Approximately 3-4 cm below the inguinal ligament, the femoral nerve divides into anterior and posterior divisions. The anterior division has two sensory branches that supply the antero medial thigh, and two muscular branches that supply the sartorius and pectineus muscles. The posterior division has one sensory branch, the saphenous nerve, and muscular branches to the quadriceps. The nerve is covered by the iliac fascia, which separates it from the main vessels, and more superficially by the fascia lata, the deep fascia of the thigh. The muscular branch to the rectus femoris also supplies the hip joint while 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 the ventral rami of spinal nerves L2-L3-L4. It emerges on the medial side of the psoas muscle just above the pelvic brim running down between this muscle and the lumbar spine. As the nerve enters the pelvis it turns laterally to run along its lateral wall until it reaches the obturator foramen, through which it reaches the thigh. In the thigh the nerve divides into anterior and posterior branches, as shown in figure 7-3.
Fig 7-3. Obturator nerve. The obturator nerve (OB) comes out of the obturator foramen where its two branches eventually straddle the adductor brevis muscle (AB). Also shown are femoral nerve (FN), femoral artery (FA), femoral vein (FV), pectineus (Pec), obturator externus (OE) and adductor longus (AL).Cadaver dissection by Dr Franco. Image is copyrighted.
The anterior division runs caudally, first located between the pectineus muscle in front and the obturator externus behind. A few cm distally the nerve runs between the 116 | P a g e
adductor longus anteriorly and the adductor brevis posteriorly. 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. The posterior division after a short trajectory it usually pierces the obturator externus to then run caudally between the adductor brevis in front and the adductor magnus behind. 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 cutaneous branch of the obturator nerve has contributed to the confusion about how much anesthesia can be obtained from a single block performed at the femoral level (“3-in-1 (“3-in-1”” block). Most of the studies have used pinprick testing of the medial, anterior and lateral thigh to assess anesthesia of obturator, femoral and lateral femoral cutaneous nerves territories. This testing does not take into account the fact that many variations exist in the innervation patterns of the thigh including the absence of a cutaneous branch of obturator nerve. Nevertheless many authors believe that a block at the femoral level could also produce anesthesia of the lateral femoral cutaneous nerve by lateral diffusion of the local anesthetic under the (“2-in-1 1 block”). block”). Spread of local anesthetic to the obturator nerve either, fascia iliaca (“2-inmedially under the vessels or proximally toward the pelvis is more unlikely. Sciatic nerve It is the largest nerve in the body. It originates from the ventral rami of spinal nerves L4-L5, S1-S3. 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 form the sciatic nerve. The nerve has two components, the tibial nerve (on its medial side), which is derived from the anterior divisions of the ventral rami of L4-L5, S1-S3 and the common peroneal nerve (on its lateral side), which is derived from the posterior divisions of the ventral rami of L4-L5, S1-S2. The nerve comes out of the pelvis through the greater sciatic foramen, entering the gluteal region anterior (deep as seen from the gluteal region) to the piriformis muscle. The nerve curves above the ischial tuberosity and then turns vertically downwards to run between the ischium medially and the greater trochanter laterally, as shown in figure 7-4.
Fig 7-4. The sciatic nerve (1) enters the gluteal region covered superficially by the piriformis muscle (2). It then travels parallel to the midline (5), between the ischium (3) and greater trochanter (4). Cadaver dissection by Dr Franco. I mage is copyrighted.
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For most of its trajectory in the buttocks, the sciatic nerve runs parallel 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, not being influenced by gender or body weight. This previously unknown fact has simplified enormously the approach to the sciatic nerve in our practice (for more information see Franco. Anesthesiology 2003; 98: 723-728). The tibial and common peroneal components can be easily identified as two separate nerves during their entire trajectory in about 11% of the cases. However, even in those cases the two components are surrounded by a common sheath of connective tissue, as shown in figure 7-5. Therefore, it is important not to confuse this with a true separation of the components, which invariably takes place always in the popliteal fossa.
Fig 7-5. The sciatic nerve components, components, tibial (T) and common peroneal (CP) share a common sheath. Cadaver dissection by Dr Franco. Image is co ri hted.
The sciatic nerve enters the thigh deep to the biceps femoris muscle and not lateral to it as usually mentioned in our literature, as shown in figure 7-6.
Fig 7-6. The sciatic nerve (SN) enters the thigh under the cover of gluteus maximus (sectioned) and biceps, which is shown split between two arrows. Cadaver dissection by Dr Franco. Image is copyrighted.
As opposed to what happens in the gluteal region, the position of the sciatic nerve in the thigh 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.
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The nerve runs in the posterior thigh under the cover of the hamstring muscles, until it reaches the popliteal fossa. Upon entering the popliteal fossa, the two nerve components, peroneal and tibial, finally diverge from each other, having never mixed their fibers. The posterior tibial nerve continues to run in the direction of the main trunk, at the center of the fossa. The common peroneal component turns laterally to run just medial to the biceps tendon, as shown in figure 7-7.
Fig 7-7. The sciatic nerve division after soft tissue removal. The sciatic nerve (SN) divides into its two components, tibial (TN) and common peroneal (CP), in the popliteal fossa. Also shown are the popliteal vein (PV), popliteal artery (PA) and muscles including semimembranosus (SM). Cadaver dissection by Dr Franco. Image is copyrighted.
Subgluteal fold The fold that defines the buttocks inferiorly is a fold of the skin and does not correspond 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 as it runs laterally to insert in the iliotibial tract, as shown in figure 7-8. Therefore, during a subgluteal approach to the sciatic nerve, the needle crosses the same planes (fat and gluteus maximus) than in more proximal approaches, although the fat layer can be thinner.
Fig 7-8. The subgluteal fold. fold . The inferior border of the gluteus maximus and subgluteal fold are two different things. They cross each other diagonally. Cadaver dissection by Dr Franco. Image is copyrighted.
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Genitofemoral nerve It derives from the ventral rami of spinal nerves L1-L2. Its genital branch provides some of the innervation of the genital area, while its femoral component provides sensory innervation of the medial upper thigh and the skin over the femoral vessels. Posterior cutaneous nerve of the thigh It is also known as posterior femoral cutaneous nerve. It originates from the ventral rami of spinal nerves S1-S3. It exits the pelvis through the greater sciatic foramen, first medial and then superficial to the sciatic nerve. Somewhere caudal to the ischium, the nerve pierces the deep fascia (fascia lata) and becomes a superficial structure. It is not a branch of the sciatic nerve, although it has a close relationship with it in the gluteal area, as shown in figures 7-9 and 7-10, before it becomes a superficial nerve as shown in figure 7-11.
Fig 7-9. The posterior femoral cutaneous nerve shown with arrows is in close contact to the sciatic nerve (SN) in the gluteal area. The sheath of the nerve is partially intact. Cadaver dissection by Dr Franco. Im Ima e is is co co ri hted.
Fig 7-10. The posterior femoral cutaneous nerve shown with arrows and sciatic nerve (SN) after removal of connective tissue. Cadaver dissection by Dr Franco. Ima e is co ri hted.
Fig 7-11. The posterior femoral cutaneous nerve becomes a superficial nerve around the subgluteal fold, where it is separated from the sciatic nerve which at this point is running under the hamstring muscles and fascia lata. Cadaver dissection by Dr Franco. Image is copyrighted.
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The posterior femoral cutaneous nerve innervates the lower part of the buttocks as well as the posterior thigh, frequently reaching as far down as the proximal posterior aspect of the leg. A block of the sciatic nerve performed in the gluteal area will predictably produce anesthesia of this cutaneous nerve as well. A block performed at the subgluteal level on the other hand, will not reliably block it. Saphenous nerve It is a sensory nerve that originates from the posterior division of the femoral nerve (L3-L4) in the inguinal region. It is the largest cutaneous branch of the femoral nerve. It runs down the femoral canal 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, as shown in figure 7-12
Fig 7-12. The saphenous nerve (SN) emerges on the medial side of the knee between sartorious and gracilis to run along the greater saphenous vein on the medial side of the leg. ATT: anterior tibial tuberosity. Cadaver dissection by Dr Franco. Image is copyrighted.
At a variable distance caudal to the knee, it pierces the deep fascia to become superficial. Distal to the knee it gives off the subpatellar branch, which supplies the medial side of the knee (chance for injury during knee arthroscopy). Once it becomes superficial, it runs alongside the greater saphenous vein in the leg, passing in front of the medial malleolus in the ankle, before terminating around the base of the first metatarsal on the medial side of the foot. Male and female pelvis issue The female pelvis is adapted to accommodate child bearing and as a result the pelvic cavity or inner pelvis is wider in females than in males. However, the total width of the bony pelvis, that is the diameter between both iliac crests (bicrestal diameter), is similar in both sexes, measuring an average of 280 mm in males and 275 mm in females (see Cunningham’s Cunningham ’s Anatomy reference). The thicker bones in the male pelvis compensate for a “roomier” female pelvis pelvis (see Hollinshead’s Anatomy reference). According to some anthropologists (Hall et al reference ) the human bony pelvis is “surprisingly” similar in males and females at all ages. The perceived 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 due to differences in the total width of the bony pelvis. It is the latter what determines the position of the sciatic nerve in the buttocks as I will discuss further when I describe the gluteal approaches to the sciatic nerve.
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Clinical pearls
The nerves of the lower extremity are more distant from each other than in the upper extremity so it is not possible to block the entire lower extremity from a single injection point. The position of the sciatic nerve in the buttocks with respect to the midline is dictated by the bony pelvis and as such it 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 rd the subgluteal fold (Snell’s ( Snell’s Clinical Anatomy for Medical Students, 3 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 gluteus maximus is the only gluteal muscle to cover the sciatic nerve superficially, caudal to the piriformis muscle in the gluteal region. Gluteus medius and minimus are located cephalad and lateral to the sciatic nerve. The inguinal crease does not correspond 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.
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LATERAL FEMORAL CUTANEOUS NERVE BLOCK Indications This block can be performed alone to provide anesthesia of the lateral thigh (e.g., donor area for a skin graft). It can also be performed along with femoral, obturator and sciatic blocks to provide anesthesia of the thigh for surgical procedures above the knee and for thigh tourniquet. It is also one of the nerves targeted in a “3-in“3-in-1” 1” block, a block of the femoral nerve performed with a higher volume of local anesthetic to try to block also the lateral femoral and obturator nerves (not supported by the evidence). Point of contact with the nerve The nerve is approached as it emerges from under the inguinal ligament, medial 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 at 2 or more cm distal to 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. ANATOMICAL TECHNIQUE 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 lata where the local anesthetic is injected in a fanwise fashion. A nerve stimulator with pulse duration of 0.3 to 1 msec (300 to 1000 microsec) can be used to elicit a sensory 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, as ropivacaine, can be used if necessary. Complications Very rare. Some patients can complain of dysesthesia in the lateral thigh that usually goes away without sequelae. ULTRASOUND TECHNIQUE The use of ultrasound facilitates this block. As the lateral femoral cutaneous nerve passes under the inguinal ligament it is located under the fascia lata in between tensor fascia lata laterally and sartorius medially. Placing the probe across the gap in between these two muscles usually allows a good visualization. A few centimeters distal to the inguinal ligament the nerve can be located superficial to the sartorius muscle.
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FEMORAL NERVE BLOCK NERVE STIMULATOR TECHNIQUE 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 usually approached just below the inguinal crease. However, if possible, the nerve can be approached immediately above the crease (1 cm), where it is more compacted, before its branches start to diverge. 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. Patient position and landmarks The patient lies supine. If necessary, the back of the bed can be slightly elevated for patient’s comfort. If done in combination with a sciatic nerve block, we prefer to do the sciatic block first because this block has a longer onset time than the femoral. The femoral pulse at the inguinal crease is found by palpation. The point of entrance is marked on the skin, proximal or distal to the inguinal crease, about 2 cm lateral to the pulse of the femoral artery, as shown in figure 7-13.
Fig 7-13. Patient position and landmarks. The patient is supine or semi seated. The location of the femoral artery (A) is found by palpation. The femoral nerve (N) is lateral to the artery, while the femoral vein (V) is medial to it. Also shown is the anterior superior iliac spine (ASIS). (On a model with permission).
Type of needle A 5 cm, 22G, insulated needle usually suffices. Nerve stimulator settings The nerve stimulator is set to deliver a 1.0 mA current, at a frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec).
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Needle insertion The needle is inserted 1-2 cm lateral to the pulsation of the femoral artery with a 30-45-degree cephalad orientation, as shown in figure 7-14 A and B.
Fig 7-14 A. Needle insertion, frontal view. The needle is inserted lateral to the artery, about 1 cm above the inguinal crease and in a 30-45 degree cephalad orientation. (On a model with per mission).
Fig 7-14 B. Needle insertion, lateral view. The needle is inserted lateral to the artery, about 1 cm above the inguinal crease and in a 30-45 degree cephalad orientation. (On a model with permission).
The needle is advanced parallel to the midline 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 and with a muscle twitch still visible at 0.5 mA a slow injection is started. A response from the sartorius is usually considered not a good response, because it could be the result of stimulation of the nerve to the sartorius, a branch of the anterior division of the femoral nerve. If the block is performed 1 cm above the inguinal crease, where the nerve has not branched off yet, a twitch from the sartorius is equally acceptable. Local anesthetic and volume The femoral nerve is a collection of branches flat in the frontal plane that offers a large area of absorption. For anesthesia we usually use 10-20 mL of 1.5% mepivacaine plus 1:400,000 epinephrine for 3-4 hours of surgical anesthesia. For longer anesthesia 0.5% ropivacaine with epinephrine can be used. For analgesia we usually use 10-15 mL of 0.2% ropivacaine. We always use epinephrine 1:400,000 as an intravascular marker. Side effects and complications Blocks at the femoral level are usually well tolerated and complications are rare.
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FEMORAL NERVE BLOCK ULTRASOUND TECHNIQUE Indications The same indications than for nerve stimulator techniques. Patient position The patient is either supine or semi seated for more comfort. Type of needle Usually a 5cm, 22-G, insulated needle is used. Type of transducer The femoral nerve is fairly superficial in most of patients, so a high frequency (815 MHz) linear probe is usually adequate. Scanning The probe is placed across the upper thigh over the femoral vessels, as shown in figure 7-15.
Fig 7-15. Femoral Scanning. The probe is placed across the neurovascular bundle, right above the crease to obtain a short axis view of the femoral nerve and vessels. (On a model with permission).
If possible we like to place the probe immediately (1 cm) above the crease, where the nerve is more compacted. The femoral vein is the most medial structure of the neurovascular bundle and is easily collapsible by the probe. The artery is situated lateral to the vein and the femoral nerve is located lateral to the artery. The characteristic image obtained at this level is shown in figure 7-16.
Fig 7-16. Femoral scanning. The femoral nerve (FN) is seen as a flat structure over the iliopsoas muscle and lateral to the femoral artery (FA). Author’s archive.
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Needle insertion The needle can be advanced out of plane, usually from caudal to cephalad, as shown in figure 7-17, or, as we usually prefer, in plane from lateral to medial, as shown in figure 7-18.
Fig 7-17. Needle insertion, out of plane. The needle is inserted from distal to proximal (cephalad direction) towards the femoral nerve. (On a model with permission).
Fig 7-18. Needle insertion, in of plane. The needle is inserted in plane from lateral to medial towards the femoral nerve. (On a model with permission).
Local anesthetic and volume The multiple branches that constitute this nerve provide an ample area of absorption for the local anesthetic. Usually we use no more than 20 mL of local anesthetic solution and as little as 10 mL in some occasions. For shorter cases 1.5% mepivacaine plus 1:400,000 epinephrine provides 3-4 hr of anesthesia. For longer cases 0.5% ropivacaine plus epinephrine is used. For analgesia 0.2% ropivacaine is our drug of choice. Side effects and 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.
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OBTURATOR NERVE BLOCK NERVE STIMULATOR TECHNIQUE Indications It is rarely performed alone. It is more often combined with femoral, lateral femoral and/or sciatic blocks. Point of contact with the nerve The needle is inserted, if possible, immediately (1 cm) above the inguinal crease to approach the nerve just distal to the obturator foramen before its two main branches diverge. Main characteristics Although the obturator nerve exits the obturator foramen usually already divided into anterior and posterior branches, they both run for a short distance (2-3 cm) physically contiguous in the plane between the pectineus anteriorly and the obturator externus posteriorly. After reaching the lateral border of the adductor brevis muscle both branches separate, with the anterior branch passing anterior to this muscle and the posterior branch posterior to it. It is a common practice to perform separate injections of both branches. However we believe that if the injection is attempted 1 cm above the crease both main branches of the obturator nerve can be blocked by a single injection deep to the pectineus muscle. Patient position and landmarks The patient lies supine with the head of the bed slightly elevated. The thigh is slightly abducted and externally rotated. Many methods have been devised to locate the obturator nerve. Our own method is to use as the main landmark the pulsation of the femoral artery. To locate the right obturator nerve the operator uses the right hand and for the left obturator the left hand. The middle finger is used on both sides to palpate the pulse of the femoral artery. This way the index finger on either side always points to the femoral nerve, the ring fingers to the femoral vein and the little finger to the obturator nerve, as shown in figure 7-19.
Fig 7-19. Finding the obturator nerve. Our own method to locate the obturator nerve uses the femoral artery pulse, which is palpated using the operator’s middle finger of the same side to be blocked (right hand to palpate right side, left hand to left side). This way the little finger will always roughly indicate the position of the obturator nerve (pointed with an arrow). (On a model with permission).
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Type of needle Depending on the patient, a 5cm, 22-G or a 10cm, 21-G, insulated needle is used. Nerve stimulator settings The nerve stimulator is set to deliver a 1.0 mA current, at a frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion The needle is inserted almost perpendicular to the frontal plane with a slight cephalad angulation, as shown in figure 7-20.
Fig 7-20. Needle insertion. The needle is inserted immediately above the inguinal crease, almost perpendicular to the frontal plane, with a slight cephalad orientation. (On a model with permission).
As the needle traverses the muscular plane, a localized twitch from the pectineus muscle is usually elicited by direct stimulation. As the needle reaches the deep face of the muscle and the proximity of the obturator nerve a more global twitch of the thigh in adduction is obtained. At this point the current is lowered progressively to around 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 A volume of 10-15 mL of local anesthetic is usually used. Mepivacaine 1.5% can be used with 1:400,000 epinephrine for 3-4 hr of anesthesia. For longer anesthesia 0.5% ropivacaine with epinephrine can be used. For analgesia 0.2% ropivacaine is commonly used. Complications Hematoma is the most frequent complication of this technique. Adductor muscles spasm can occur.
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OBTURATOR NERVE BLOCK ULTRASOUND TECHNIQUE Indications The same indications mentioned for nerve stimulator techniques. Patient position The patient lies supine with the head of the bed slightly elevated. The thigh is slightly abducted and externally rotated. Type of needle Depending on the patient, a 5cm, 22-G or a 10cm, 21-G, insulated needle is used. Type of transducer If at all possible a high frequency (8-15 MHz) linear probe is used. Scanning Before performing the scanning it is useful, if possible, to locate the adductor longus, the most superficial of the three adductor muscles, as shown in figure 7-21.
Fig 7-21. Identifying the adductor longus muscle. With the thigh in slight abduction and slight external rotation the adductor longus (AL) can usually be easily palpated. (On a model with permission).
This way the determination of the location of the obturator nerve is framed between two easily identifiable structures, the femoral vessels on the lateral side and the medial border of the adductor longus on the medial side. The probe is placed parallel and slightly above the inguinal crease over the femoral vessels and then traced medially until it rests over the pectineus muscle, as shown in figure 7-22.
Fig 7-22. Scanning the obturator nerve. The probe is place across the femoral vessels, as done for femoral block, and then slowly displaced medially until it rests over the pectineus muscle, just cephalad to the inguinal crease. (On a model with permission).
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With the probe over the pectineus muscle the obturator nerve can be seen as a mostly hyperechogenic ovoid image under the pectineus muscle, as shown in figure 7-23.
Fig 7-23. Obturator nerve, proximal view. With the probe just medial to the femoral vein (FV) and just above the crease, the obturator nerve (arrow) appears as an oval hyperechoic structure under the pectineus muscle. (FV). Author’s archive.
If the scanning instead is performed a few centimeters more distally then the two branches of the obturator can be seen, as shown in figure 7-24.
Fig 7-24. Obturator nerve, distal view. With the probe below the inguinal crease the two main components (arrows) of the obturator nerve can be seen above and below the adductor brevis (AB). Adductor longus (AL), adductor magnus (AM) also shown. Author’s archive.
Needle insertion My preferred method for this particular block is to use and out of plane technique from distal to proximal, as shown in figure 7-25.
Fig 7-25. Needle insertion. The needle is introduced out of plane, from distal to proximal. On a model with permission).
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Local anesthetic and volume A volume of 10-15 mL of local anesthetic is usually used. Mepivacaine 1.5% can be used with 1:400,000 epinephrine for 3-4 hr of anesthesia. For longer anesthesia 0.5% ropivacaine with epinephrine can be used. For analgesia 0.2% ropivacaine is commonly used. Complications Hematoma is the most frequent complication of this technique. Adductor muscles spasm can occur.
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LUMBAR PLEXUS BLOCK (also called “psoas compartment block”) NERVE STIMULATOR TECHNIQUE Indications Its goal is to produce anesthesia of the lateral femoral, femoral and obturator nerves, so it can be used along with a proximal sciatic nerve block to provide anesthesia of the entire lower extremity. It is also used to provide postoperative analgesia for hip and knee surgery. Point of contact with the nerve(s) The plexus is accessed deeply in the lumbar area in the space limited by the quadratus lumborum posteriorly (more superficial or closer to the skin of the back) and the psoas muscle anteriorly (deeper). Main characteristics “3-in-1” 1” block in block in the femoral area intends to It is the posterior version of what a “3-inaccomplish. It is a deep block, in which the needle goes through several layers, including subcutaneous tissue, the mass of paraspinal muscles, and the quadratus lumborum muscle before ending just posterior to the psoas muscle, in the retroperitoneal space. Because of the depth at which the nerves are located and the long needles used, the operator has little control over the exact location of the needle tip, increasing the potential risk for complications. The most frequent complication is to produce an epidural block, but also cases of total spinal anesthesia have been described. Because of the relatively large volumes of local anesthetics used systemic toxicity can also develop. Cases of penetration of the peritoneal cavity with injury of its contents as well as large retroperitoneal hematomas and death have been reported with this block. It is essential that the operator be familiar with the anatomy of this region before attempting this block, which should be performed only by experienced people. The lumbar plexus block perhaps 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 a neuraxial block. A line is drawn at the level of the iliac crest (L4-L5 interspace) starting at the midline (spinous processes) and extending to the level of the posterior superior iliac spine. The line is then divided into thirds, as shown in figure 7-26.
Fig 7-26. Landmarks. A line at the level of the iliac crests is drawn from the midline to the PSIS and divided into thirds. The junction of the lateral and middle thirds is the point of needle insertion shown with an arrow. On a model with permission).
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Type of needle At least a 10cm, 21-G, insulated needle is necessary for this block. Nerve stimulator settings The nerve stimulator is set to deliver a current of 1.5 mA, at a pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion The needle is inserted parallel to the midline at the junction between the lateral third and middle third of the line joining the midline with the level of the posterior superior iliac spine, as shown in figure 7-27.
Fig 7-27. Needle insertion. The needle is inserted at the junction between the lateral and middle thirds of the line drawn from the midline to the PSIS, and directed parallel to the midline. On a model with permission).
This insertion is more medial than the original technique. It is based on a study by Capdevila et al (Anesth Analg 2002; 94: 1606-1613) demonstrating that the point of needle insertion at the level of the PSIS falls lateral to the plexus mandating a medial reposition of the needle that potentially could increase the chance for epidural or spinal anesthesia. As the needle is inserted through the mass of the paraspinal muscles a local contraction is usually observed. The transverse process of L4 or the nerves of the lumbar plexus should be contacted within 3 cm from the disappearance of the twitch from the back muscles. If not, the needle is withdrawn superficially and redirected caudally or cephalad. If the transverse process is contacted the needle should be walked off caudally until a quad twitch is obtained, usually no deeper than 2 cm from the transverse process. If no response is obtained within 2 cm the needle can be redirected cephalad from the transverse process and again advanced for up to 2 cm. When a muscle twitch from the quad is obtained the current in the nerve stimulator is decreased to around 0.5-0.8 mA and with a visible response a gentle 3-5 mL aspiration is performed for blood or CSF befor e injecting a “test dose” amount of 3-5 of epinephrine-containing local anesthetic. If no intravascular or subarachnoid injection is detected the rest of the local anesthetic volume is slowly injected in small increments with frequent gentle aspirations. The preferred response in this block is quad response. An obturator response could mean that the needle is too medial and should be redirected. A distal response (sciatic) could mean that the lumbosacral trunk is being stimulated and could indicate a needle too medial. A medial position of the needle could carry an increased risk of neuraxial injection. 134 | P a g e
Local anesthetic and volume For anesthesia of 3-4 hours 1.5% mepivacaine with epinephrine 1:200,000 (a larger concentration than we use at other sites) can be used. For longer anesthesia the preferred drug is 0.5% ropivacaine plus 1:200,000 epinephrine. For analgesia 0.2% ropivacaine is adequate. Complications I already mentioned that this block should be performed only by experienced people. Epidural spread is the most common problem with an incidence of 1-16%, but can be as high as 88% in some reports. Subarachnoid injection is a dangerous complication not always avoided by a test dose. Death associated with total spinal has been reported. Large retroperitoneal hematomas are also possible and therefore this block should adhere to the same anticoagulation guidelines than neuraxial techniques. Kidney and other injuries have also been reported. LUMBAR PLEXUS BLOCK ULTRASOUND TECHNIQUE The ultrasound technique is based on the ability to map the sonoanatomy of the lumbar spine and associated muscles. Because of the depth of these structures a curved, low frequency probe is used. The technique can be “ultrasound assisted” rather than ultrasound guided.
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SCIATIC NERVE BLOCK Classic approach (Labat as modified by Winnie) NERVE STIMULATOR TECHNIQUE Indications As an isolated block, 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 (lumbar plexus block), it completes the anesthesia of the entire lower extremity. Point of contact with the nerve The nerve is contacted in the gluteal area at the point where it is entering the gluteal area caudal to the piriformis muscle. The needle on occasions could traverse through the piriformis. Main characteristics Labat’s approach is a highly anatomical anatomical approach that requires the identification of the posterior superior iliac spine (PSIS) and the greater trochanter (GT). A dissection of the gluteal area shows that this is a reliable approach if the operator is able to accurately determine the position of the PSIS and GT, disregarding ANY soft tissue (i.e., muscle, bursa, subcutaneous tissue and fat). Position of the patient and landmarks The patient is positioned in lateral decubitus, with the side to block up. The dependent leg is extended. The non-dependent leg is flexed at the hip and at the knee, while the buttock the buttock is rotated anteriorly (Sim’s position). The PSIS is marked and so is the superior aspect of the GT. The midpoint of this PSIS-GT transverse line is determined. From this midpoint a perpendicular line measuring 3 cm, is directed caudally and medially. This is the point of needle insertion. It is important that the marks placed on the skin truly represent the posterior projection of the bony prominences on the skin. Marking the position of the GT on the lateral buttock for example, would artificially lengthen the PSIS-GT line (because of soft tissue), making its midpoint artificially more lateral and away from the sciatic nerve. The 3-cm perpendicular line has also been a source of problems. Several authors have modified its length to a range of 2 to 5 cm. In 1974 Winnie and collaborators published in Anesthesiology Review a modification to the Labat’s Labat ’s technique. This modification has been universally adopted and it is now commonly known as the “classic” technique. In order to deal with the controversy about the appropriate length of Labat’s original 3-cm perpendicular line, they proposed to draw an additional transverse line extending from the sacral hiatus (SH) to the tip of the greater trochanter to provide a distal point of intersection for the perpendicular line of Labat. In this manner, the length of this line would be determined by the distance between the two transverse lines, and wou ld be “self adjustable” to every particular patient. Quoting the authors, “with this technique the distance along the perpendicular line will vary with the height of the patient”. This apparent solution is
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widely accepted but it might have some problems of its own. Because, as discussed in the anatomy section, the transverse diameter of the pelvis is fairly constant in all adults, any prolongation of the perpendicular line starting from a similar point would bring it closer to the midline (its direction is caudal and medial). This will mean that a tall patient with a long sacrum will have a sciatic nerve located closer to the midline (long perpendicular line due to longer sacrum) than a short patient (short perpendicular line due to shorter sacrum). This obviously could not b e the case. The fact is that Labat’s perpendicular line was not created to be adjustable. The combined “classic” approach (Labat-Winnie), 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 10cm, 21-G, 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 For anesthesia 1.5% mepivacaine plus 1:400,000 epinephrine in a volume of 3035 mL can provide 3-4 hrs of anesthesia. Ropivacaine 0.5-0.75% with epinephrine can be used if longer duration is needed. 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, therefore hematomas could develop. The patient lying supine immediately post block could theoretically help to decrease the chance for a hematoma to develop. It is important to inject slowly, alternated with frequent and gentle aspirations. Dysesthesias in the territories of the sciatic or posterior femoral cutaneous nerves are reported more frequently after this block than any other. These problems usually resolve spontaneously within 1-2 weeks.
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SCIATIC NERVE BLOCK Franco’s approach NERVE STIMULATOR TECHNIQUE Indications The same indications than for a classic technique. Point of contact with the nerve This is a mid-gluteal technique that approaches the sciatic nerve distal to the piriformis in the proximity of the ischium at about the same level than the classic technique does. However, because caudal to the piriformis the sciatic nerve runs almost parallel to the midline, this technique can be performed at any point between mid-gluteal to subgluteal levels. It can also be used for continuous catheter techniques. Main characteristics This is a simple technique that relies on one simple anatomical landmark, the intergluteal sulcus (midline), making the palpation of any buried landmarks totally unnecessary. It is based on simple, although 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 according to some anthropologists “surprisingly” similar in males and females at any given age. Variations in hip width are mainly the result of hormone-dependent, different patterns of fat deposition in both sexes and are not due to significant differences in the width of the bony pelvis. Although male and female pelvises are indeed different, most of those differences are limited to the diameters of the minor or inner pelvis without affecting the total diameter of the pelvis. Thicker bones in 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. As determined by our own study (Anesthesiology 2003; 98: 723-728), the sciatic nerve is located about 10 cm from the midline (intergluteal sulcus) in all adults. What remains highly variable is the amount of adipose tissue that can accumulate in the buttocks affecting the depth of the nerve and its distance to the lateral side of the patient. The distance midline-nerve is, on the other hand, unaffected by fat accumulation as it is dictated by the distance between the ischium and the midline (fixed after puberty). Position of the patient and landmarks This block can be performed in the lateral decubitus or in the prone position. We prefer to do it almost 100% of the times in the lateral position, because it is more comfortable for the patient and faster to prepare for. The patient is placed in the lateral position with both hips and knees slightly flexed. In a true lateral decubitus, a tangential line to the buttocks, should form a 90-degree angle with the table. Having the patient placed at straight angles with the table, makes his/her midline parallel to the table.
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The midgluteal sulcus is identified and the point of needle insertion is marked at 10 cm from it around the midgluteal region, as shown in figure 7-28.
Fig 7-28. Patient position and point of needle insertion. insertion. 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).
This is a linear measurement that, on purpose, disregards any particular curvature or contour in the patient’s buttocks. The insertion point, always located at 10 cm from the midline, can be moved distally at will, as far caudal as the subgluteal fold. This could be necessary for example, if the buttock is large and the needle is not long enough. Type of needle A 10cm, 21-G, insulated needle is usually sufficient, although in some cases a 15cm needle is necessary. Nerve stimulator settings For this technique we set the nerve stimulator current at 1.5 mA (1.8 mA in diabetic patients), with a frequency of 1 Hz and pulse duration of 0.1 ms (100 microsec). Needle insertion The needle is advanced parallel to the midline, as shown in figure 7-29.
Fig 7-29. Needle insertion. The needle is inserted parallel to the midline.(On a patient with permission).
When the needle reaches the gluteus maximus muscle a local muscular twitch of the buttock is observed. 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 cm or more, of a 10 cm needle, have been used to reach the gluteus maximus, it is unlikely that the needle will be long enough to reach the sciatic nerve. 139 | P a g e
The needle is advanced through the gluteus muscle, producing a visible local twitch that does not disappear until the needle exits the deep surface of this muscle. The ensuing “silence” is evidence that the needle is passing through the connective tissue that separates the gluteus maximus from the nerve. It 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 and against eversion. This is not our experience. If no response from the sciatic nerve is obtained deeper to the gluteus maximus, then a reposition of the needle is necessary. Here is very important to take into account the “vector” effect, the impact of the angle of reinsertion in the final position of the needle. According to my own calculations, at a theoretical depth of 9 cm, a 10-degree correction angle, moves the needle tip 1.6 cm, while a 20-degree correction moves it 3.4 cm. Because the nerve is around 1.5 cm wide, it would be 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 before reaching 0.5 mA the twitch becomes too weak, the current is not lowered any further and instead the operator slowly moves the needle closer to the nerve. It is not infrequent to see the response fade as the needle is inserted deeper. This can be the result of a needle approaching the nerve tangentially, overshooting the nerve on one of its sides. In these cases we usually like to perform a small correction in order to get a “bull’s eye” alignment 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 nerve (lateral side), while inversion and plantar flexion are responses from the tibial nerve (medial side). A small correction is then made accordingly. A more controlled correction can be accomplished by only partially removing the needle a couple of cm. The unburied portion of the needle is then bent and directed in the desired direction. The buried portion of the needle keeps the needle from overcorrecting. Bringing the needle out completely, and then reinserting it, carries a chance of overshooting the correction.
Complications Same as classic approach. Pearls
The 10 cm measurement is a linear measurement that disregards, on purpose, the contour of the patient’s buttock . This linear measurement tries to reflect only the distance between the midline and the outer lip of the ischium, without soft tissue interference. Placing the patient in true lateral position, makes the patient’s midline parallel to the table. If this position is not possible, the operator needs to ascertain the degree 140 | P a g e
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 to underestimate the midline-nerve distance (sagging midline). Therefore, the first correction should be lateral. When reposition is necessary, 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 20degree 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.
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MIDGLUTEAL SCIATIC BLOCK ULTRASOUND TECHNIQUE Indications The same than for nerve stimulation techniques. Patient position For a midgluteal approach the patient can be placed prone, lateral or in Sim’s position. Type of needle A 10 or 15cm, 21-G, insulated needle is used. Type of transducer Because of the depth at which the sciatic nerve is located in the gluteal area, most of the times a curved, low frequency (5-7 MHz) probe is needed. Scanning The nerve is identified in cross section (short axis) by placing the transducer across the midgluteal area at which point the sciatic nerve can be identified between the greater trochanter and ischial tuberosity, as shown in figure 7-30.
Fig 7-30. Sciatic nerve scanning. With the probe in the midgluteal region the sciatic nerve (SN) is observed between the greater trochanter (GT) and ischial tuberosity (IT). Author’s archive.
Needle insertion The easiest approach is to introduce the needle out of plane from distal to proximal as observed in figure 7-31.
Fig 7-31. Needle insertion. The needle is inserted out of plane from distal to proximal. On a model with per mission).
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Figure 7-32 shows an ultrasound image of an out of plane technique during injection.
Fig 7-32. Sciatic nerve injection. Out of plane technique. The sciatic nerve (SN) is shown in between greater trochanter (GT) and ischial tuberosity (IT). The tip of the needle is shown above the nerve pointed with an arrow and the injected local anesthetic appears as a dark hypoechoic shadow on top of the nerve. Author’s archive.
Local anesthetic and volume For anesthesia 1.5% mepivacaine plus 1:400,000 epinephrine provides 3-4 hr of anesthesia. For longer duration 0.5% ropivacaine can be used. For analgesia 0.2% ropivacaine is appropriate. Complications The same as nerve stimulation techniques.
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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 can also be used for continuous catheter techniques. Point of contact with the nerve The nerve is approached in the vicinity of the subgluteal fold. Main characteristics There are several 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, not subgluteal level), just a few cm caudal to Labat’s classic approach. In this technique the extremity 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”, approach”, a completely similar technique was published a year earlier (1974) by Winnie and colleagues in Anesthesiology Review. Raj’s technique was below-the-knee knee operations”. This fact is frequently forgotten and correctly devised “for below-thewe will revisit it later. A popular infra or subgluteal technique is the technique introduced by di Benedetto and colleagues in 2001. Patient position and landmarks This block is performed in the Sim’s position, position , as the classic technique. The greater trochanter and the ischium are identified and a line is drawn in between the two. The midpoint of this line is determined. A second line is drawn from this midpoint, perpendicularly and caudally for 4 cm. This is the needle insertion point. According to the authors, the operator should be able to palpate at this point a “skin depression”, which would represent “the groove between the biceps femoris and semitendinosus muscles”. This groove supposedly represents the trajectory of the sciatic nerve. This is just one more instance in which anesthesiologists display their love affair with grooves. In fact cadaver dissections show:
1. Ischium and greater trochanter are located at about the same transverse plane in the buttocks, as shown in figure 7-1. 7- 1. Di Benedetto’s perpendicular line going caudal and lateral, needs to have the trochanter located significantly higher than the ischium. 2. The subgluteal fold is about 8 cm caudal to the midpoint between ischium and greater trochanter and not 4 cm. On the other hand, being the subgluteal fold so evident, would it suffice to extend the line until it intercepted the subgluteal fold? 3. At the subgluteal fold the three components of the hamstring muscles are practically fused together in one single tendon, without any evident groove in 144 | P a g e
between. More distally in the thigh a groove can be found between biceps and semitendinosus, but it is too subtle to be easily palpable through several layers of tissue (skin, subcutaneous tissue and thick fascia lata). 4. A groove is visible in most people between the biceps and the iliotibial tract. This groove has nothing to do with the trajectory of the sciatic nerve. 5. The sciatic nerve runs under the biceps femoris and not in a groove between biceps and semitendinosus. Technique The authors suggest to insert the needle perpendicular to the skin until a twitch from the sciatic nerve is obtained. Local anesthetic and volume The same than for classic approach Complications Common to other approaches to the sciatic nerve.
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SCIATIC NERVE BLOCK, SUBGLUTEAL Franco’s approach
The subgluteal approach can be easily performed at 10 cm from the midline at the subgluteal fold, with the patient lying in lateral decubitus, as shown in fig 7-33.
Fig 7-33. Needle insertion point. point. It is easily found at 10 cm from the midline as done for the midgluteal approach. (On a patient with permission).
The 10-cm measurement is made from the midline at the level of the subgluteal fold, in a way similar to the one described for the mid-gluteal approach. The needle is advanced parallel to the midline, through the gluteus maximus muscle and into 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. The needle is reinserted, with a small 10-degree correction in its orientation, first lateral (toward the trochanter) and then medial (to the midline) if necessary. Ultrasound technique Although the same tissue layers cover the sciatic nerve at the midgluteal and subgluteal levels, the fat layer is usually thinner. This makes the ultrasound visualization of the sciatic nerve at this level usually easier than in the midgluteal area. Depending on depth, the nerve can be visualized with a linear high frequency probe, but frequently a lower frequency probe is needed. Curved low frequency probes are needed for bigger patients. The patient is placed prone, lateral position or in Sim’s position. The nerve is visualized in cross section (short axis) and the needle is advanced either out of plane (usually) or in line with the probe. 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 (our own data, Reg Anesth Pain Med 2006; 31: 215-20). The reason is that the posterior femoral nerve is usually already a superficial nerve (above the fascia) at the level of the subgluteal fold. 2. The inferior border of gluteus maximus and subgluteal fold are not the same thing. Therefore, during a subgluteal approach the needle needs to pass through the same layers of tissue than at more proximal approaches. 146 | P a g e
3. The sciatic nerve is relatively more superficial at the subgluteal fold because the amount of fat decreases from mid-gluteal to subgluteal level, although the type of layers (fat and muscle) remains the same. 4. The popliteal fossa is the only level in the trajectory of the sciatic nerve in which the nerve is not covered superficially by muscle. Approaching the sciatic nerve, without passing through muscle is the only true advantage of a popliteal approach. 5. In terms of anesthesia distribution, the subgluteal approach is more comparable to the popliteal block than to other more proximal approaches.
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SCIATIC NERVE BLOCK, POPLITEAL Franco’s approach NERVE STIMULATOR TECHNIQUE Indications It is especially suitable for foot surgery. Along with femoral nerve block (saphenous) it provides complete anesthesia below the knee. Point of contact with the nerve The needle approaches the sciatic nerve high in the popliteal fossa, before its main components diverge from each other. Main characteristics This is the only place in the trajectory of the sciatic nerve where the nerve is not covered superficially by muscle, perhaps its only true advantage over other more proximal approaches to the sciatic nerve. Characteristically, a sciatic block done at this level with a blind technique has a slower onset and lower success rate than more proximal approaches. The fact that the two components of the nerve diverge from each other could account for some of the partial blocks. However, slower onset and lower success rates are sometimes observed in cases where there is reasonable evidence to believe that the main trunk has been contacted. One of the possible reasons is that the nerve sheath at this level fuses with the fat that fills the popliteal fossa soaking the local anesthetic away from the nerve. Ultrasound techniques have a faster onset. Patient position and landmarks This block is most usually performed in the prone position. T he patient’s patella is palpated with two hands, to verify the neutral position of the knee on the bed (the natural resting position of the knee is with a small degree of lateral rotation). The patient is then asked to flex the knee slightly to make the biceps (lateral) and semitendinosus (medial) tendons visible at the popliteal crease. A mark is placed on both tendons at the crease, as shown in figure 7-34.
Fig 7-34. Landmarks. Landmarks. The biceps and semitendinosus tendons (ST) are marked at the crease. (On a model with permission).
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The distance between these two points in adults is usually 6-7 cm in females and 7-8 cm in males. The midpoint between the two tendons is located and marked, as shown in figure 7-35.
Fig 7-35. Inter tendinous distance. The midpoint between biceps and semitendinosus tendons is determined at the crease. (On a model with ermission).
The needle insertion point is then found 7-9 cm above the crease, as shown in figure 7-36.
Fig 7-36. Point of needle insertion. The point of insertion shown with an arrow, is found 7-9 cm above the midpoint of the tendons at the crease. (On a model with permission).
Type of needle A 5cm, 22-G, insulated needle is usually adequate. Nerve stimulator settings The nerve stimulator is set to deliver a current of 1.0 mA (higher in diabetics) with a pulse frequency of 1 Hz and pulse duration of 0.1 msec (100 microsec). Needle insertion The needle is introduced with a 30-45 degree cephalad orientation, as shown in figure 7-37.
Fig 7-37. Needle insertion. The needle is inserted with a cephalad orientation. (On a model with permission).
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The needle is directed approximately 45-degrees cephalad, so the contact with the nerve happens at 1-2 cm higher from the crease than the actual entrance point, increasing the chances that the sciatic nerve is contacted prior to its division. The distance from the crease at which the needle is inserted varies according to the patient’s height. A good ballpark estimation is to insert the needle at a distance from the crease that is 1 cm longer than the intertendinous distance. Once a response from the sciatic nerve is elicited, and still present at 0.5 mA or less, a slow injection is started with frequent aspirations. Local anesthetic and volume I believe that a block of the sciatic nerve in the popliteal fossa using nerve stimulation requires a higher volume than more proximal approaches. As a general rule I give about 10 mL more of local anesthetic solution than what I would give to the same patient at more proximal locations. This comes to about 35-45 mL of 1.5% mepivacaine with 1:400,000 epinephrine for 3-4 hr of anesthesia. If longer anesthesia is desired I would use 10 mL of 1.5% mepivacaine with epinephrine followed by 30 mL of 0.5% ropivacaine. Complications Small hematoma can develop. Residual dysesthesia lasting up to two weeks can be seen.
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POPLITEAL BLOCK, LATERAL APPROACH WITH NERVE STIMULATOR Indications It is especially suitable for any surgery below the knee including ankle and foot, in patients who cannot be placed in any other position than supine Point of contact with the nerve Similar to the posterior technique. The needle approaches the sciatic nerve from the lateral side, before this nerve’s main components diverge from each other. The needle is advanced between the biceps (posteriorly) and vastus lateralis (anteriorly) into the popliteal fossa. Main characteristics Blocking the sciatic nerve with this approach is a little bit more challenging than the posterior approach. Biceps and vastus lateralis fibers are in close physical contact so the needle usually stimulates some muscle fibers before reaching the sciatic nerve. Patient position and landmarks The patient lies supine in the semi sitting position. A pillow is placed under the leg, so the hip and knee are slightly flexed. The patient can be asked to shift his/her weight to the opposite side, so a small degree of lateral rotation is obtained. The popliteal crease is identified and marked toward the lateral side of the knee. The cleavage between the biceps and vastus lateralis is identified. A mark is placed in this groove 10 cm proximal to the popliteal crease. This is the point of needle insertion. Technique The midpoint of the patella is found and a line is drawn from it proximally into the thigh. This line represents roughly the projection of the sciatic nerve and therefore it can be used to estimate the depth of the sciatic nerve, as measured from the lateral side. With the thigh in slight lateral rotation the needle is advanced with a 30-degree posterior orientation. A local twitch of biceps and/or vastus lateralis muscles can be found before entering the popliteal fossa. If the needle overshoots the projection of the nerve without eliciting a twitch, it is withdrawn to the skin and a small 10-degree posterior correction is applied before reinsertion. With a visible twitch at 0.5 mA or less, a slow injection is started with frequent aspirations. Local anesthetic and volume The same than for posterior approach. Complications The same than for posterior approach.
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POPLITEAL BLOCK ULTRASOUND TECHNIQUE Indications The same indications than nerve stimulation techniques. Patient position There are basically two main positions in which this block can be performed, supine and prone. The views obtained are similar, but in general the supine technique can be more challenging, especially in larger patients. The supine technique usually involves an in-plane lateral approach, while the prone technique provides the opportunity for out of plane approaches also. Whether the technique is done supine or prone, having the patient flex the knee improves the visualization of the sciatic nerve and its components. Type of needle If an out of plane technique is performed usually a 5cm, 22-G, insulated needle suffices. If an in plane lateral approach is attempted usually a longer 10cm, 21-G, insulated needle is needed. Type of transducer In most cases a linear, high frequency (8-15 MHz) is used. In larger patients it is sometimes necessary to use a curved, low frequency (3-7 MHz) probe. Scanning The nerve is scanned in short axis. The scanning can be started at any level in the popliteal fossa, but it is helpful to start at the crease where the popliteal vessels, vein and artery, have an intimate relationship with the tibial component of the sciatic nerve. Figure 7-38 shows a sequence of images as the probe is moved from distal to proximal. Fig 7-38, A and B. Popliteal scanning. Image A (left) obtained at the crease shows vein (PV), artery (PA) and tibial nerve (arrow). Figure B (right) shows both components of the sciatic nerve (arrows) . Author’s Author’s archive.
Fig 7-38, C and D. Popliteal scanning. Image C (left) shows both components approaching each other (arrows). Figure D (right) shows the sciatic nerve (SN) as a single structure. Author’s archive.
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Needle insertion The needle can be inserted out of plane, usually from distal to proximal or in plane from lateral to medial, as shown in figure 7-39.
Fig 7-39. Needle insertion, supine technique. The needle is inserted in plane, from the lateral side in the groove between vastus lateralis and biceps. (On a model with permission).
A needle inserted in plane from the lateral side is easily seen in the screen as shown in figure 7-40.
Fig 7-40. Popliteal block, in plane technique. The needle (shown with 2 arrows) is seen approaching the sciatic nerve (SN) from the lateral side. The injected local anesthetic is seen as a hypoechoic (dark) lagoon surrounding the nerve. Author’s archive.
Local anesthetic and volume For surgery 30-40 mL of 1.5% mepivacaine can provide 3-4 hr of anesthesia. For longer cases 30 mL of 0.5% ropivacaine with epinephrine can be used. For analgesia 0.2% ropivacaine is adequate.
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References rd
1. Snell RS: Clinical anatomy for medical students, 3 edition. Boston, MA: Little, Brown and Company; 1986 2. Labat G: Regional anesthesia: Its technique and clinical application. Philadelphia, PA: W.B. Saunders, 1922 3. Shipman P, Walker A, Bichell D: Human skeleton. Cambridge, MA: Harvard University Press; 1985 4. Hall J, Froster-Iskenius U, Allanton J: Handbook of normal physical measurements. Oxford: Oxford University Press; 1989 5. Cunningham’s Textbook of Anatomy, 5th edition. Edited by Robinson A. New York, William Wood and Company, 1928, pp 258 6. Hollinshead’s Textbook of Anatomy, 5th edition. Edited by Rosse Rosse C, GaddumRosse P. Philadelphia, Lippincott-Raven, 1997, pp 641 – 641 – 80 80 7. Winnie A, Ramamurthy S, Durrani Z, et al. Plexus blocks for lower extremity surgery. Anesthesiology Review 1974; 1: 11-16 8. Franco, CD. Posterior approach to the sciatic nerve in adults: Is Euclidean geometry still necessary? Anesthesiology 2003; 98: 723-728 9. Franco CD, Choksi N, Rahman A, Voronov G, Almachnouk M. A Subgluteal Approach to the Sciatic Nerve in Adults at 10 cm from the Midline. Reg Anesth Pain Med 2006; 31: 215-20 10. Di Benedetto P, Bertini L, Casati A, et al. A new approach to the sciatic nerve block: A prospective, randomized comparison with the classic posterior approach. Anesth Analg 2001; 93: 1040-1044 11. Rogers J, Ramamurthy S: Lower extremity blocks, Regional anesthesia and analgesia. Edited by Brown DL. Philadelphia, PA: W.B. Saunders Company, 1996 rd 12. Mulroy M: Regional Anesthesia, An illustrated procedural guide, 3 edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2002 13. Enneking FK, Chan V, Greger J, et al. Lower-extremity peripheral nerve blockade: Essentials of our current understanding. Reg Anesth Pain Med 2005; 30: 4-35 14. Vloka JD, Hadzic A, Drobnik L, Ernest A, Reiss W, Thys DM. Anatomical landmarks for femoral nerve block: A comparison of four needle insertion sites. Anesth Analg 1999; 89: 1467-1470 15. Capdevila X, Macaire P, Dadure C, Choquet O, Biboulet P, Ryckwaert Y, D’Athis F. Continuous psoas compartment block for postoperative analgesia after total hip arthroplasty: New landmarks, technical guidelines, and clinical evaluation. Anesth Analg 2002; 94: 1606-1613 16. Orebaugh SL. The femoral nerve and its relationship to the lateral circumflex femoral artery. Anesth Analg 2006; 102: 1859-1862
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CHAPTER 8 CONTINUOUS NERVE BLOCKS
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Introduction
Single-shot peripheral nerve blocks provide quality anesthesia for a variety of different procedures. In most cases postoperative pain is moderate and manageable with either IV PCA (patient controlled analgesia) or oral analgesics. However, there are surgical procedures known to be followed by intense pain in the postoperative period. Pain is a very important and usually not well addressed problem. It does not only affect patients physically and emotionally, but also affects their recovery time and rehabilitation. In those cases in which postoperative pain is expected to be more than moderate and lasts longer than the duration of a single shot block, the anesthesiologist needs other means to produce and prolong the analgesia. Ideally, analgesia could be provided by slow-released analgesic products injected along with local anesthetics during single shot techniques. Local anesthetics and other substances like morphine have been added to liposome systems to deliver controlled and steady doses of analgesia. However, to date only duromorph, a liposomal system delivering morphine, is the only one available. It has been approved by the FDA for epidural analgesia. In this context continuous peripheral nerve blocks with perineural catheters become an excellent option for postoperative analgesia providing the versatility in duration and effect that single shot techniques lack. F. Paul Ansbro published in 1946 what is widely considered the first account of a continuous peripheral nerve block technique. He described a technique in the supraclavicular area in which he used a needle passed through a cork for stabilization. Once the needle was inserted to an adequate level, as judged by paresthesia, the cork was advanced to the level of the skin and taped. A tubing connected to a syringe provided the opportunity for what Ansbro called “fractional injections”. More recently in the 1970s, Selander introduced continuous techniques in the axillary region using an IV cannula left in place. Benefits of continuous perineural catheters
Many authors have demonstrated the benefits of continuous techniques, mainly prolonged analgesia without the undesirable side effects associated with opioid use (i.e., nausea, vomiting, constipation, dependency), better patient satisfaction and better ability to participate in rehabilitation. Liu and Salinas published in 2003 an excellent review on continuous perineural blocks. After an extensive review of the available literature they concluded that there was enough evidence to support the claim of superior analgesia of continuous perineural blocks as compared to IV PCA “for open shoulder procedures and total knee replacement”. It is likely that may other surgical procedures could also benefit from the ability to extend the analgesia provided by perineural catheters. Continuous techniques
Continuous blocks are usually performed in a similar way than single-shot techniques with the addition of a catheter that provides the means to continuously deliver the analgesic solution. Single-shot blocks (“primary block”) are generally associated with 156 | P a g e
a high success rate. Catheters techniques (“secondary block”) do not generally achieve the same degree of success. Catheters need to be closely placed in the proximity of target nerve(s) in order to decrease the “secondary block failure”, a failure to achieve the same degree of success than single shot techniques. In general catheters should not be advanced more than 3-4 cm because the risks for catheter-related complications (e.g., knotting, vascular puncture, nerve injury, etc) potentially increase. Stimulating versus non-stimulating catheters
There are proponents of both techniques. The non-stimulating catheters are commonly inserted through an insulated, Tuohy type needle. The catheter can be a single orifice catheter in which the hole is usually at the tip, or most commonly a multiorifice catheter with a dead end (no hole at the tip) and three side holes, the distal one at about 0.5 cm from the tip. The proximal hole is separated from the distal one by a distance of about 1 cm. After the needle is positioned the catheter is advanced to the desired location. The technique is generally easy, but the success of the secondary block (through the catheter) depends on a good perineural placement of the catheter. The stimulating catheter uses for insertion a similar Tuohy type needle, but the catheter itself has a wire connected to its tip, allowing for stimulation through it in a similar fashion than through a needle. The ability to stimulate a nerve as the catheter is advanced provides a measure of catheter tip-nerve proximity. If the elicited twitch disappears the catheter is carefully withdrawn into the housing of the needle to avoid cutting or otherwise damaging the catheter. The position of needle is then slightly modified by rotation or by moving it in and out a few millimeters and a new attempt is made. The needle and catheter together as a unit can be slightly rotated in its main axis before reinserting the catheter. This technique can be more time consuming and more difficult, but supposedly decreases secondary failure. The introduction of ultrasound into regional anesthesia practice with its ability to visualize the needle and catheter as well as the spread of the local anesthetic solution, has called into question the need for stimulating catheters. Catheter related problems
The most common problems with catheters include inability to achieve adequate analgesia and other technical problems like accidental dislodgement and peri-catheter own”. They can advance away from nerves leaks. Catheters tend to have a “mind of their own”. and into undesirable places. Capdevila et al in 2005 in a multicenter study that included 1,416 patients identified 17.9 % of “technical problems due to catheters and devices”. Many techniques are used to increase the resistance to accidental dislodgement. Perhaps the most successful is the subcutaneous tunnelization of the catheter. It does not only increase the resistance to removal but also provides the opportunity to direct the catheter away from the surgical site. Severe nerve damage and infection are rare complications of continuous techniques.
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References
1. Ansbro FP. A method of continuous brachial plexus block. Am J Surg 1946; 71: 716722 2. Selander D. Catheter technique in axillary plexus block. Acta Anaesthesiol Scand 1977; 21: 324-329 3. Liu SS, Salinas FV. Continuous plexus and peripheral nerve blocks for postoperative analgesia. Anesth Analg 2003; 96: 263-272 4. Boezaart AP: Continuos Peripheral Nerve Blocks, In: Boezaart AP (ed): Anesthesia and Orthopaedic Surgery. New York, McGraw-Hill, 2006, pp 257-264 5. Capdevila X, Pirat P, Bringuier S, et al. Continuous peripheral nerve blocks in hospital wards after orthopedic surgery: A multicenter prospective analysis of the quality of postoperative analgesia in 1,416 patients. Anesthesiology 2005; 103: 10351045
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CHAPTER 9 OTHER NERVE BLOCKS
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TRANS ABDOMINAL PLANE (TAP) BLOCK
The innervation of the anterolateral abdominal wall is provided by the lower six th thoracic (intercostal) nerves and the first lumbar nerve. The 7 intercostal nerve swings up and terminates around the xiphoid of the sternum in the highest point of the abdominal th th wall. The 10 intercostal runs almost horizontally toward the umbilicus, while the 12 intercostal (subcostal) innervates the area above the inguinal ligament and suprapubic area. The first lumbar nerve originates the iliohypogastric and ilioinguinal nerves, both branches of the lumbar plexus, which run above the iliac crest. Main characteristics This block was described before the use of ultrasound. It was performed in the posterior abdominal wall at the level of the triangle of Petit. This triangle is formed anteriorly by the posterior border of the external oblique muscle, posteriorly by the anterior border of latissimus dorsi and inferiorly by the iliac crest. The area of the triangle is covered superficially by the aponeurosis of insertion of the external oblique and deeper by the external oblique and transversus abdominis muscles. The performance of this block used to require the feeling of “pop” sensations as the needle crossed the different fascia and muscle planes. Since the introduction of ultrasound I recommend doing this block under direct vision. Indications To produce anesthesia or analgesia of the abdominal wall. Point of contact with the nerves The needle approaches the thoraco abdominal nerves as they travel between the transversus abdominis (deep) and the internal oblique (superficial) muscles at the level of the mid axillary line. Patient position The patient can be supine or in lateral position with the arm on the side to be blocked elevated and turned to the opposite side. Type of needle A 5cm, 22-G, insulated needle is usually used. An 18-G epidural needle can also been used with the advantage that the bigger needle is more readily seen and its curved end could help minimize the accidental puncture of deeper planes. Type of transducer A linear high frequency (8-15 MHz) probe is usually sufficient. In larger patients with thicker abdominal wall (more fat) a curved, low frequency (3-7 MHz) probe is necessary. Scanning The probe is placed diagonally over the lateral abdominal wall at the level of the mid axillary line.
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Needle insertion The needle can be inserted in plane or out of plane. We prefer to insert the needle in plane from anterior to posterior, as shown in figure 9-1.
Fig 9-1. Needle insertion, in plane. The needle is inserted in plane, from anterior to posterior. (On a model with p ermission).
The planes observed at this level are shown in figure 9-2.
Fig 9-2. TAP block. With the probe placed diagonally over the lateral abdominal wall, the external oblique (EXT), internal oblique INT) and transversus abdominis (TRA) are easily distinguished. The arrows show the fascial plane between the internal oblique and transversus muscles where the injection is erformed. Author’s archive.
Local anesthetic and volume A volume of 15 to 20 mL on one or bilateral is used according to the incision site. This block produces somatic pain relief (abdominal wall incision) but it does relieve visceral pain. For analgesia 0.2% ropivacaine plus epinephrine is frequently used.
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References th
1. Snell RS: Clinical anatomy for medical students, 5 edition. Boston, MA: Little, Brown and Company; 1986, pp 133-182 2. Rafi A. Abdominal field block: A new approach via the lumbar triangle. Anaesthesia 2001; 56: 1024-26. 3. Hebbard P, Fujiwara Y, Shibata Y, Royse C. Ultrasound-guided transversus abdominis plane (TAP) block. Anaesthesia and Intensive Care 2007; 35: 616-7. 4. Carney J, McDonnell JG, Ochana A, et al. The transversus abdominis plane block provides effective postoperative analgesia in patients undergoing total abdominal hysterectomy. Anesth Analg 2008; 107:2056-60 5. McDonnell JG, Curley G, Carney J, et al. The analgesic efficacy of transversus abdominis plane block after cesarean delivery: A randomized controlled trial. Anesth Analg 2008; 106:186 – 106:186 – 91 91
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