Donald H. Lambert

Cauda Equina Syndrome and Continuous Spinal Anesthesia

In this report, we present pictures produced with a spinal canal model to demonstrate how neural damage might occur with continuous spinal anesthesia. The hypothesis is based on the fact that nerves exposed to large volumes of 5% lidocaine solution may be damaged

Role of needle gauge and tip configuration in the production of lumbar puncture headache

Background and Objectives. Postdural puncture headache (PDPH) is a morbidity that occurs frequently after lumbar puncture. The purpose of this study was to evaluate the role of needle diameter and tip configuration in causing PDPH. The incidence of PDPH was evaluated in parturients because this group of patients is at high risk for developing PDPH and because they often undergo lumbar puncture for spinal anesthesia. Methods. The incidence of PDPH after spinal anesthesia with 26‐ and 27‐gauge Quincke and 25‐gauge Whitacre needles was studied in a series of 4,125 parturients undergoing spinal anesthesia over a 4‐year period. Data were also collected on the incidence of PDPH with 17‐gauge Huber‐tipped Weiss needles in 21,578 parturients receiving lumbar epidural analgesia and/or anesthesia over the same interval. Additionally, the need to treat PDPH with epidural blood patch in all of these patients was studied. Results. The incidence of PDPH was 5.2% with 26‐gauge Quincke needles (1987‐1989), 2.7% with 27‐gauge Quincke needles (1989‐1990), and 1.2% with 25‐gauge Whitacre needles (1990‐1991). During the same periods, the incidence of PDPH with 17‐gauge Weiss needles averaged 1.1%, 1.7% and 1.2%, respectively. As compared with the 26‐gauge Quincke needle, there was a lower incidence of PDPH with the 27‐gauge Quincke (P < .006) and 25‐gauge Whitacre spinal needles (P < .001). The incidence of PDPH with the 25‐gauge Whitacre needle was less than that with the 27‐gauge Quincke needle (P < .05), and it was similar to the overall rate of headache, which occurs occasionally from accidental dural puncture during the performance of lumbar epidural analgesia/anesthesia for labor and cesarean delivery (P = .974). The need for treating PDPH with epidural blood patching was greatest with the 17‐gauge Weiss epidural needle (75.3% of cases), but was similar with the various spinal needles (13‐39%). However, because the Whitacre needle produced the fewest PDPHs, it was associated with the lowest absolute requirement for epidural blood patching. Conclusions. The morbidity associated with lumbar puncture can be decreased by selecting the proper needle gauge and tip configuration. Use of the smallest gauge needle and one that has a noncutting Whitacre tip produces the lowest incidence of PDPH in parturients, a group of patients at increased risk for developing PDPH.

Continuous Spinal Anesthesia with a Microcatheter Technique: Preliminary Experience

This report describes the evolution of the microcatheter, the problems encountered during its initial utilization, the intricacies involved with insertion and removal, and our results with 58 patients

The search for an optimal interval between pretreatment dose of D-tubocurarine and succinylcholine

A study was conducted to determine the optimal interval between the administration of d-tubocurarine (dTc) and succinylcholine (SCh) with regard to onset and duration of neuromuscular block and presence of fasciculations and postoperative myalgias.Forty female patients received dTc 3 mg .70kg-1 prior to SCh 1.5mg.kg-1. The interval between drugs was 0, I, 3, 5, or 7 minutes Transduced thumb adduction recorded block onset and recovery. Fasciculations were visually detected. Myalgias were assessed on postoperative interview.Pretreatment interval did not affect the onset or recovery of neuromuscuiar block. Postoperative myalgias were also independent of pretreatment timing. Fasciculations were blocked with 3, 5, or 7 minute intervals, but not with Oor I minute intervals. Therefore, three minutes appear to be the optimal, time interval between administration of dTc and SCh since shorter intervals do not inhibit fasciculations and longer intervals do not afford any additional advantages.RésuméOn a cherché à déterminer I’mtervalle idéal à maintenir entre l’administration préventive de la d-lubocurarine (dTc) et celle de la succinytcholine (SCh), intervalle qui permettruit de conserver la rapidité d’ installation du bloc neuromusculaire et sa durée tout en minimisanl ies fasciculations et Ies myalgies post-opératoires.L étude a porté sur 40 patientes ayant reçu 3 mg 70 kg-1 de dTc avant I’administration de 1.5 mg-kg-1 SCh. Les patientes ont été réparties en groupes ou l’intervalle entre I’administration des médicaments a été de O, 1, 3, 5, et 7 minutes. La mesure de l’adduction du pouce par transducteur moniwrait I installation et la disparition du bloc neuromusculaire. Les fasciculations etaient observées visuellement et les myalgies évaluées au cours d’une entrevue post-opératoire.L’installation ou la disparition du bloc neuromusculaire n’est pas influencée par I’intervalle entre les injections non plus que les myalgies post-operatoires. Les fasciculations étaient éliminées pour des intervalles de 3, 5 ou 7 minutes maix encore présentes pour des intervcdles de 0 ou I minute.Il semble done qu’un intervalle de trot’s minutes entre I administration de dTc et de SCh est souhaitable car des intervalles plus courts ne préviennent pas les fasciculations et des intervalles plus longs n’opponent aucun avantage additionnel.

Clinical value of adding sodium bicarbonate to local anesthetics

niques used to identify the brachial plexus; we fully concur with his opinions. The technical simplicity, the objective end point in identifying the brachial plexus, and the outcome of block have undoubtedly contributed to make neurostimulation the gold standard in plexus anesthesia. Furthermore, Dr. Sia introduces the idea of multiple neurostimulation as a technique capable of affording an increased success rate in relation to plexus block, with a reduction in latency. The recent work by Sia et al.1 and Serradell-Catalán et al.2 attempt to answer the question: “How many responses must we identify?” In the study by Sia et al.,1 comparing the identification of 2 or 3 responses to neurostimulation in the axillary technique, the authors conclude that the identification of 2 responses (radial and median) may suffice for surgery of the hand, whereas surgery of the forearm would require the added identification of the musculocutaneous nerve. Similar results have been reported by Serradell-Catalán et al.2 in which comparisons were made of 5 groups of 20 patients with multiple neurostimulatory responses, suggesting the need to identify 3 motor responses (including that of the musculocutaneous nerve) for securing a block rate of 90%. In this same study, the identification of 4 terminal nerves secured a complete block in 100% of cases. However, caution is indicated when interpreting these results as definitive. The complication rate related to neurostimulation techniques should be considered in the context of epidemiologic studies involving a sufficiently large and specifically designed series of patients. These studies will be clearly larger than those needed to simply assess success of the technique. Although extensive clinical series suggest that the incidence is indeed similar for both approaches (i.e., multiple and single stimulation),3 Serradell-Catalán et al.2 have reported an increased incidence of vascular punctures when attempting to elicit an increased number of motor responses. In sum, 2 views can be identified in the conduct of plexus anesthesia: (1) classic single-stimulation techniques, considering the existence of the aponeurotic sheath and the presence of a neurovascular space; and (2) the application of the advantages of neurostimulation, in which selective block of the terminal nerve is regarded as a technique affording an increased success rate. Both views are undoubtedly valid and can coexist. Although multiple terminal-nerve neurostimulatory techniques yield increased complete block rates, the single techniques offer the possibility of selective anesthetic reinforcement limited to nonblocked nerve branches. In our opinion, neurostimulation provides greatest localization of the neurostimulation needle, and therefore of the local anesthetic instillation close to the brachial plexus. Based on the location of multiple muscle responses, using the knowledge of the most common muscle responses of the different terminal nerves, we can improve the outcome of block. However, the needle puncture remains blind in that we know the puncture site, “imagine” the trajectory, and identify the location of the plexus. This may imply an increased risk of complications associated with these multiple punctures. Moreover, considerable interindividual anatomical variability exists as regards the location of the different “end-nerves” in relation to the axillary artery.4 Systematic application in the near future of imaging techniques, such as ultrasound,5 may afford improvements, causing a “partially blind” multiple stimulation procedure to transform into a technique performed under direct and continuous visualization, thereby securing its 2 fundamental objectives, i.e., the best possible block result with the fewest puncture-associated complications.

Reply to Dr. Moore.

1. Pollock JE. Transient neurologic symptoms: An update. Reg Anesth Pain Med 2002;27:581-586. 2. Wong C, Benzon H, Kim C. Bilateral radicular pain after epidural lidocaine. Reg Anesth 1996;21:600-601. 3. Markey JR, Naseer OB, Bird DJ, et al. Transient neurologic symptoms after epidural analgesia. Anesth Analg 2002;90:437439. 4. Hiller A, Rosenberg P. Transient neurologic symptoms after spinal anaesthesia with 4% mepivacaine and 0.5% bupivacaine. Br J Anaesth 1997;79:301-305. 5. Salmela L, Aromaa U. Transient radicular irritation after spinal anesthesia induced with hyperbaric solutions of cerebrospinal fluid-diluted lidocaine 50 mg/ml or mepivacaine 40 mg/ml or bupivacaine 5 mg/ml. Acta Anaesthesiol Scand 1998; 42;765-769. 6. Liguori GA, Zayas VM, Chisholm M. Transient neurologic symptoms after spinal anesthesia with mepivacaine and lidocaine. Anesthesiology 1998;88:619-623. 7. Salazar R, Bogdanovich A, Adalia R, Chabas E, Gomar C. Transient neurologic symptoms after spinal anesthesia using isobaric 2% mepivacaine and isobaric 2% lidocaine. Acta Anaesthesiol Scand 2001;45:240-245.

Cardiac arrest during neuraxial anesthesia: are all databases comparable?

1. The Closed Claims Database (CCDB) (2,3) is 60 times larger than Kopp’s. 2. The outcome at the Mayo Clinic should be better than at the varied hospitals represented in the CCDB, where fewer resources are available compared with a tertiary care facility. 3. The distribution of serious outcomes in the CCDB does not necessarily match those from a single institution’s sample. 4. Because the CCDB arose from malpractice claims, there can be no meaningful statistical comparisons with the Mayo Clinic’s, where cases not involving a malpractice claim are equally likely to be included as those that do.

Is continuous spinal anesthesia really so bad

We had a 14-yr-old man (177 cm, 70 kg) with potassium chloride (KCl)-resistant severe hypokalemia, which developed during an emergency aortic arch replacement under deep hypothermic cardiopulmonary bypass. Because of the persisting intermittent bilateral convulsive waves on his electroencephalograms, the cumulative dose of thiamylal reached 30 mg/kg. The serum concentration of potassium decreased to 1.6 mEq/L, and the urine concentration decreased to 1.3 mEq/L. His hypokalemia did not respond to an aggressive supplement of KC1 up to 80 mEq/h (the total dose reached 190 mEq), but it did respond to a substitution of midazolam for thiamylal. This clinical course raises the possibility that thiamyla1 may have contributed to his severe hypokalemia. Schalen et al. (1) have reported that 21% of their brain-injured patients undergoing thiopental coma therapy developed severe hypokalemia below 2 mEq/L with a concomitant decrease in urinary output of potassium. Anesthesiologists should be aware that barbiturate therapy might cause or exacerbate hypokalemia. Whether this type of hypokalemia has detrimental effects on organ functions or some beneficial effects on maintaining intracellular potassium content should be also elucidated. Does the latter play a role for its protective effects on cerebral ischemia?